Many of the patients attend after thorascopic sympathectomy which resolved their palmar, but not axillary, hyperhidrosis. Surgical excision of axillary tissue remains an important treatment modality for a large proportion of hyperhidrotic patients. It has the ability to provide a permanent and satisfactory solution to a frustrating problem. It is not as yet a redundant method of treatment.
J L Atkins, senior house officer, plastic surgery.
P E M Butler, consultant plastic surgeon.
Royal Free Hospital, London NW3 2QG
BMJ 2000;321:702 ( 16 September )
Letters
Treating hyperhidrosis
Excision of axillary tissue may be more effective
Monday, May 5, 2008
Skin in 'overdrive' following sympathectomy
I. Kelman Cohen1 Contact Information and Barbara J. McCoy1
(1) Division of Plastic Surgery, Department of Surgery, Medical College of Virginia, 23298 Richmond, Virginia, USA
Lesions of “surface overhealing” include keloid, hypertrophic scar, and burn scar. All are characterized by overabundant collagen deposition. The biology of these lesions is reviewed, suggesting that abnormal collagen metabolism results from alterations in the inflammatory/immune response. Practical and theoretical treatment plans are outlined based on methods that alter collagen metabolism, the inflammatory/immune system or rely on physical alterations (surgery, pressure).
(1) Division of Plastic Surgery, Department of Surgery, Medical College of Virginia, 23298 Richmond, Virginia, USA
Lesions of “surface overhealing” include keloid, hypertrophic scar, and burn scar. All are characterized by overabundant collagen deposition. The biology of these lesions is reviewed, suggesting that abnormal collagen metabolism results from alterations in the inflammatory/immune response. Practical and theoretical treatment plans are outlined based on methods that alter collagen metabolism, the inflammatory/immune system or rely on physical alterations (surgery, pressure).
Saturday, May 3, 2008
Structural changes and in situ aortic pressure-diameter relationship
These results suggest that intact sympathetic nerves are necessary to maintain normal functional and structural properties of large arteries in rat. The reduction in aortic distensibility, in long-term sympathectomized rats, could have resulted from complex interactions between local aortic denervation, change in the set point of distending pressure, and changes in aortic smooth muscle tone and/or wall composition.
Auteur(s) / Author(s)
LACOLLEY P. ; GLASER E. ; CHALLNDE P. ; BOUTOUYRIE P. ; MIGNOT J.-P. ; DURIEZ M. ; LEVY B. ; SAFAR M. ; LAURENT S. ;
American journal of physiology. Heart and circulatory physiology ISSN 0363-6135 COD
1995, vol. 38, no2, pp. H407-H416 (36 ref.)
Auteur(s) / Author(s)
LACOLLEY P. ; GLASER E. ; CHALLNDE P. ; BOUTOUYRIE P. ; MIGNOT J.-P. ; DURIEZ M. ; LEVY B. ; SAFAR M. ; LAURENT S. ;
American journal of physiology. Heart and circulatory physiology ISSN 0363-6135 COD
1995, vol. 38, no2, pp. H407-H416 (36 ref.)
Friday, May 2, 2008
Sequential cerebrospinal fluid and plasma sampling in humans: 24-hour melatonin measurements in normal subjects and after peripheral sympathectomy
In the patient with hyperhidrosis, a prominent melatonin rhythm was observed preoperatively in the CSF and plasma. After bilateral T1-T2 ganglionectomy, however, melatonin levels were markedly reduced, and the diurnal rhythm was abolished. These results provide direct evidence in humans for a diurnal melatonin rhythm in CSF and plasma as well as regulation of this rhythm by sympathetic innervation.
J Bruce, L Tamarkin, C Riedel, S Markey and E Oldfield
Surgical Neurology Branch, National Institute of Neurologic Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.
Journal of Clinical Endocrinology & Metabolism, Vol 72, 819-823, Copyright © 1991 by Endocrine Society
J Bruce, L Tamarkin, C Riedel, S Markey and E Oldfield
Surgical Neurology Branch, National Institute of Neurologic Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892.
Journal of Clinical Endocrinology & Metabolism, Vol 72, 819-823, Copyright © 1991 by Endocrine Society
Melatonin - Circadian Cycle - Delayed sleep phase syndrome
Main article: Circadian rhythm sleep disorder
Delayed sleep-phase syndrome (DSPS), also known as delayed sleep-phase disorder (DSPD) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder, a chronic disorder of the timing of sleep, peak period of alertness, core body temperature, hormonal and other daily rhythms. People with DSPS tend to fall asleep well after midnight and have difficulty waking up in the morning.
DSPS is a disorder of the body's timing system - the biological clock. Individuals with DSPS might have an unusually long circadian cycle, or might have a reduced response to the re-setting effect of light on the body clock.
People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with DSPS are unable to fall asleep before their usual sleep time, even if they are sleep-deprived. Research has shown that sleep deprivation does not reset the circadian clock of DSPS patients, as it does with normal people.[10]
People with the disorder who try to live on a normal schedule have difficulty falling asleep and difficulty waking because their biological clocks are not in phase with that schedule. Normal people who do not adjust well to working a night shift have similar symptoms.
People with the disorder also show delays in other circadian markers, such as melatonin-secretion and the core body temperature minimum, that correspond to the delay in the sleep/wake cycle. The timing of sleepiness, spontaneous awakening, and these internal markers are all delayed by the same number of hours. Non-dipping blood pressure patterns are also associated with the disorder when present in conjunction with socially unacceptable sleeping and waking times.
In most cases, it is not known what causes the abnormality in the biological clocks of DSPS patients. DSPS tends to run in families,[11] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[12][13] There have been several documented cases of DSPS and non-24 hour sleep-wake syndrome developing after traumatic head injury.[14][15]
There have been a few cases of DSPS developing into non 24-hour sleep-wake syndrome, a more severe and debilitating disorder in which the individual sleeps later each day.[16]
In humans, melatonin is produced by the pineal gland, a gland about the size of a pea, located in the center of the brain. The melatonin signal forms part of the system that regulates the circadian cycle by chemically causing drowsiness and lowering the body temperature, but it is the central nervous system that controls the daily cycle in most components of the paracrine and endocrine systems[23][24] rather than the melatonin signal (as was once postulated).
Delayed sleep-phase syndrome (DSPS), also known as delayed sleep-phase disorder (DSPD) or delayed sleep-phase type (DSPT), is a circadian rhythm sleep disorder, a chronic disorder of the timing of sleep, peak period of alertness, core body temperature, hormonal and other daily rhythms. People with DSPS tend to fall asleep well after midnight and have difficulty waking up in the morning.
DSPS is a disorder of the body's timing system - the biological clock. Individuals with DSPS might have an unusually long circadian cycle, or might have a reduced response to the re-setting effect of light on the body clock.
People with normal circadian systems can generally fall asleep quickly at night if they slept too little the night before. Falling asleep earlier will in turn automatically advance their circadian clocks due to decreased light exposure in the evening. In contrast, people with DSPS are unable to fall asleep before their usual sleep time, even if they are sleep-deprived. Research has shown that sleep deprivation does not reset the circadian clock of DSPS patients, as it does with normal people.[10]
People with the disorder who try to live on a normal schedule have difficulty falling asleep and difficulty waking because their biological clocks are not in phase with that schedule. Normal people who do not adjust well to working a night shift have similar symptoms.
People with the disorder also show delays in other circadian markers, such as melatonin-secretion and the core body temperature minimum, that correspond to the delay in the sleep/wake cycle. The timing of sleepiness, spontaneous awakening, and these internal markers are all delayed by the same number of hours. Non-dipping blood pressure patterns are also associated with the disorder when present in conjunction with socially unacceptable sleeping and waking times.
In most cases, it is not known what causes the abnormality in the biological clocks of DSPS patients. DSPS tends to run in families,[11] and a growing body of evidence suggests that the problem is associated with the hPer3 (human period 3) gene.[12][13] There have been several documented cases of DSPS and non-24 hour sleep-wake syndrome developing after traumatic head injury.[14][15]
There have been a few cases of DSPS developing into non 24-hour sleep-wake syndrome, a more severe and debilitating disorder in which the individual sleeps later each day.[16]
In humans, melatonin is produced by the pineal gland, a gland about the size of a pea, located in the center of the brain. The melatonin signal forms part of the system that regulates the circadian cycle by chemically causing drowsiness and lowering the body temperature, but it is the central nervous system that controls the daily cycle in most components of the paracrine and endocrine systems[23][24] rather than the melatonin signal (as was once postulated).
Reduced melatonin production has been proposed as a likely factor in the significantly higher cancer rates in night workers
Reduced melatonin production has been proposed as a likely factor in the significantly higher cancer rates in night workers,[28] and the effect of modern lighting practice on endogenous melatonin has been proposed as a contributory factor to the larger overall incidence of some cancers in the developed world.
^ Schernhammer E, Rosner B, Willett W, Laden F, Colditz G, Hankinson S (2004). "Epidemiology of urinary melatonin in women and its relation to other hormones and night work". Cancer Epidemiol Biomarkers Prev 13 (62): 936-43. PMID 15184249
^ Schernhammer E, Rosner B, Willett W, Laden F, Colditz G, Hankinson S (2004). "Epidemiology of urinary melatonin in women and its relation to other hormones and night work". Cancer Epidemiol Biomarkers Prev 13 (62): 936-43. PMID 15184249
CCS alone significantly decreased melatonin concentrations in serum at the time of highest secretory activity of the pineal gland
J. GORSKI, D. KAJDANIUK, J. GLOGOWSKA-SZELAG, Z. OSTROWSKA, M. NOWAK, B. BUNTNER
I Department of Pathophysiology and Medical Analytics, Silesian University School of Medicine, 41-800 Zabrze, Poland
The study showed that morphine alone significantly increased melatonin concentrations in serum. CCS alone significantly decreased melatonin concentrations in serum at the time of highest secretory activity of the pineal gland. Long-term morphine treatment of rats subjected to CCS significantly increased the serum concentration of melatonin. Therefore, it may be concluded that the central adrenergic system does not take part in the morphine-stimulated secretion of melatonin.
I Department of Pathophysiology and Medical Analytics, Silesian University School of Medicine, 41-800 Zabrze, Poland
The study showed that morphine alone significantly increased melatonin concentrations in serum. CCS alone significantly decreased melatonin concentrations in serum at the time of highest secretory activity of the pineal gland. Long-term morphine treatment of rats subjected to CCS significantly increased the serum concentration of melatonin. Therefore, it may be concluded that the central adrenergic system does not take part in the morphine-stimulated secretion of melatonin.
procarbazine
Sensitivity to procarbazine
»Caution should be used also in patients who have had previous cytotoxic drug therapy or radiation therapy. »In addition, caution should be used in patients who have undergone sympathectomy, who may be more sensitive to the hypotensive effects of MAO inhibitors.
Other medical problems, especially active alcoholism, bone marrow depression, cardiac arrhythmias, chickenpox or recent exposure, congestive heart failure, coronary insufficiency, severe or frequent headaches, hepatic function impairment, herpes zoster, other infection, paranoid schizophrenia or other hyperexcitable personality states, pheochromocytoma, sympathectomy, or renal function impairment
Indications
Systemic
Lymphomas, Hodgkin's (treatment) or [Lymphomas, non-Hodgkin's (treatment)]
Procarbazine is indicated, in combination with other agents, for treatment of Hodgkin's disease (Stage III and IV) and some non-Hodgkin's lymphomas .
[Tumors, brain, primary (treatment)]
Procarbazine is indicated for treatment of primary brain tumors .
[Multiple myeloma (treatment)]
Procarbazine is indicated for treatment of multiple myeloma.
»Caution should be used also in patients who have had previous cytotoxic drug therapy or radiation therapy. »In addition, caution should be used in patients who have undergone sympathectomy, who may be more sensitive to the hypotensive effects of MAO inhibitors.
Other medical problems, especially active alcoholism, bone marrow depression, cardiac arrhythmias, chickenpox or recent exposure, congestive heart failure, coronary insufficiency, severe or frequent headaches, hepatic function impairment, herpes zoster, other infection, paranoid schizophrenia or other hyperexcitable personality states, pheochromocytoma, sympathectomy, or renal function impairment
Indications
Systemic
Lymphomas, Hodgkin's (treatment) or [Lymphomas, non-Hodgkin's (treatment)]
Procarbazine is indicated, in combination with other agents, for treatment of Hodgkin's disease (Stage III and IV) and some non-Hodgkin's lymphomas .
[Tumors, brain, primary (treatment)]
Procarbazine is indicated for treatment of primary brain tumors .
[Multiple myeloma (treatment)]
Procarbazine is indicated for treatment of multiple myeloma.
Thursday, May 1, 2008
neuroaxial block may produce profound bradycardia and hypotension
A high level of neuroaxial block may produce profound bradycardia and hypotension, possibly as a result of an imbalance between sympathetic and parasympathetic control of heart rate.
Our results indicate that cervical, but not lumbar, epidural anesthesia depresses phasic and tonic dynamic modulation of the cardiac cycle by the vagal nerve in conscious humans.
IMPLICATIONS: Cervical epidural anesthesia with lidocaine produces depressed heart rate variability and baroreflex control of heart rate, whereas lumbar epidural anesthesia exerts minimal effects on autonomic nervous system activity in conscious humans.
Anesth Analg 2004;99:924-929
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000131966.61686.66
REGIONAL ANESTHESIA
The Effects of Cervical and Lumbar Epidural Anesthesia on Heart Rate Variability and Spontaneous Sequence Baroreflex Sensitivity
Makoto Tanaka, MD, Toru Goyagi, MD, Tetsu Kimura, MD, and Toshiaki Nishikawa, MD
Our results indicate that cervical, but not lumbar, epidural anesthesia depresses phasic and tonic dynamic modulation of the cardiac cycle by the vagal nerve in conscious humans.
IMPLICATIONS: Cervical epidural anesthesia with lidocaine produces depressed heart rate variability and baroreflex control of heart rate, whereas lumbar epidural anesthesia exerts minimal effects on autonomic nervous system activity in conscious humans.
Anesth Analg 2004;99:924-929
© 2004 International Anesthesia Research Society
doi: 10.1213/01.ANE.0000131966.61686.66
REGIONAL ANESTHESIA
The Effects of Cervical and Lumbar Epidural Anesthesia on Heart Rate Variability and Spontaneous Sequence Baroreflex Sensitivity
Makoto Tanaka, MD, Toru Goyagi, MD, Tetsu Kimura, MD, and Toshiaki Nishikawa, MD
Influence of sympathectomy in humans on the rhythmicity of 6-sulphatoxymelatonin urinary excretion
The amount of 6-sulphatoxymelatonin, the chief metabolite of melatonin, in the urine was measured in nine patients, who were subjected to bilateral sympathectomy at the second thoracic ganglionic level for treatment of hyperhidrosis of the palms. All patients showed before surgery a normal 6-sulphatoxymelatonin excretion with a peak in the excretion during the night time. After the sympathectomy, the high night time excretion was clearly abolished in five patients but remained high in four patients. This indicates that the segmental locations of the preganglionic sympathetic perikarya in the spinal cord, stimulating the melatonin secretion in the pineal gland in humans, vary between individuals. An increase in daytime melatonin excretion was observed in the patients responding to the sympathectomy with an abolished 6-sulphatoxymelatonin rhythm. This increase could indicate that the final sympathetic neurons innervating the pineal gland might have a both stimulatory and inhibitory function.
Morten Møllera, Corresponding Author Contact Information, E-mail The Corresponding Author, Ole Osgaardb and Michael Grønbech-Jensenc
aInst. Med. Anatomy, University of Copenhagen, Panum Institute, Blegdamsvej 3, DK-2200 Copenhagen, Denmark
bDepartment Neurosurgery, Rigshospitalet, Copenhagen, Denmark
cNeurological Specialist Clinic Copenhagen, Christianshavns Torv 2, Copenhagen, Denmark
Morten Møllera, Corresponding Author Contact Information, E-mail The Corresponding Author, Ole Osgaardb and Michael Grønbech-Jensenc
aInst. Med. Anatomy, University of Copenhagen, Panum Institute, Blegdamsvej 3, DK-2200 Copenhagen, Denmark
bDepartment Neurosurgery, Rigshospitalet, Copenhagen, Denmark
cNeurological Specialist Clinic Copenhagen, Christianshavns Torv 2, Copenhagen, Denmark
Does the pineal gland have a role in the psychological mechanisms involved in the progression of cancer?
Department of Anatomical Sciences, University of Adelaide, Adelaide, Australia
Received 9 November 2001;
accepted 13 February 2002.
Available online 28 August 2002.
Psychological factors, e.g., depression and psychological stress have been implicated in the progress of cancer. Similarly, the pineal gland and its principal secretion, melatonin, are known to influence the initiation and progress of cancer. Furthermore, changes in melatonin secretion have been linked with psychological stress and depression, and both the pineal gland and the cerebral cortex act via the limbic system in producing their effects. Both psychological stress and melatonin affect the immune system, as does the hypothalamus and the autonomic nervous system. The pineal gland has both a direct effect on cancer, and via the immune system. Psychological treatment and melatonin treatment have both been found to alleviate the course of cancer clinically. It is thus hypothesized that the pineal gland, and melatonin, are involved in the mechanism of psychological effects in the promotion of the progress of cancer.
Received 9 November 2001;
accepted 13 February 2002.
Available online 28 August 2002.
Psychological factors, e.g., depression and psychological stress have been implicated in the progress of cancer. Similarly, the pineal gland and its principal secretion, melatonin, are known to influence the initiation and progress of cancer. Furthermore, changes in melatonin secretion have been linked with psychological stress and depression, and both the pineal gland and the cerebral cortex act via the limbic system in producing their effects. Both psychological stress and melatonin affect the immune system, as does the hypothalamus and the autonomic nervous system. The pineal gland has both a direct effect on cancer, and via the immune system. Psychological treatment and melatonin treatment have both been found to alleviate the course of cancer clinically. It is thus hypothesized that the pineal gland, and melatonin, are involved in the mechanism of psychological effects in the promotion of the progress of cancer.
Two cases of symptomatic cluster-like headache suggest the importance of sympathetic/parasympathetic balance
Despite several reports on symptomatic cluster-like headache, there is no clear explanation of how different lesions thought to be causative are related to cluster-like headache. On the basis of two additional cases of symptomatic cluster headache, we discuss the possibility that an acute imbalance of the autonomic nervous system, namely a net overactivity of the parasympathetic system, may be able to trigger these headache attacks in patients who probably have an additional individual predisposition to react with a cluster-like headache. Such an imbalance can be due to an increase in parasympathetic tone (e.g. stimulation of parasympathetic fibres) or to a reduction of the sympathetic tone (e.g. a lesion of the sympathetic fibres).
Two cases of symptomatic cluster-like headache suggest the importance of sympathetic/parasympathetic balance
* A Straube,
* T Freilinger,
* T Rüther &
* C Padovan
*
Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-University Munich, Germany
----------------------------------
A chronobiological study of melatonin, cortisol growth hormone and prolactin secretion in cluster headache
Results from this study suggest a neuroendocrine dysregulation in cluster headache in the endogenous clock which controls the pineal rhythmicity.
* Guy Chazot11Unite Neurométabolique, Hôpital Neurologique. 59 boulevard Pinel, 69003 Lyon, France; ,
* Bruno Claustrat22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Jocelyne Brun22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Daniel Jordan33Laboratoire de Médecine Expérimentale, INSERM U. 197-UER, Médecine Alexis Carrel, rue Guillaume Paradin. 69008 Lyon, France; ,
* Geneviève Sassolas44Unite de Soins, Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France,
* Bernard Schott
Cephalalgia
Volume 4 Issue 4 Page 213-220, December 1984
Although migraineurs appear in general to be hypersensitive to external stimuli, they maybe also have increased daytime sleepiness and complain of fatigue. Neurophisiological studies between attacks have shown that for a number of different sensory modalities the migrainous brain is characterised by a lack of habituation of evoked responses. Whether this is due to increased cortical hyperexcitability, possibly due to decreased inhibition, or to an abnormal responsivity of the cortex due a decreased preactivation level remains disputed. Studies using transcranial magnetic stimulation in particular have yielded contradictory results. We will review here the available data on cortical excitability obtained with different methodological approaches in patients over the migraine cycle. We will show that these data congruently indicate that the sensory cortices of migraineurs react excessively to repetitive, but not to single, stimuli and that the controversy above hyper- versus hypo-excitability is merely a semantic misunderstanding. Describing the migrainous brain as ‘hyperresponsive’ would fit most of the available data. Deciphering the precise cellular and molecular underpinnings of this hyperresponsivity remains a challenge for future research. We propose, as a working hypothesis, that a thalamo-cortical dysrhythmia might be the culprit.
Is the cerebral cortex hyperexcitable or hyperresponsive in migraine?
* G Coppola11G.B. Bietti Eye Foundation-IRCCS, Department of Neurophysiology of Vision and Neurophthalmology, ,
* F Pierelli2,32University of Rome ‘La Sapienza’ Polo Pontino—I.C.O.T., Rome and 3IRCCCS-Neuromed, Pozzilli (IS), Italy, &
* J Schoenen4,5
Two cases of symptomatic cluster-like headache suggest the importance of sympathetic/parasympathetic balance
* A Straube,
* T Freilinger,
* T Rüther &
* C Padovan
*
Department of Neurology, Klinikum Großhadern, Ludwig-Maximilians-University Munich, Germany
----------------------------------
A chronobiological study of melatonin, cortisol growth hormone and prolactin secretion in cluster headache
Results from this study suggest a neuroendocrine dysregulation in cluster headache in the endogenous clock which controls the pineal rhythmicity.
* Guy Chazot11Unite Neurométabolique, Hôpital Neurologique. 59 boulevard Pinel, 69003 Lyon, France; ,
* Bruno Claustrat22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Jocelyne Brun22Service de Radiopharmacie et Radioanalvse. Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France; ,
* Daniel Jordan33Laboratoire de Médecine Expérimentale, INSERM U. 197-UER, Médecine Alexis Carrel, rue Guillaume Paradin. 69008 Lyon, France; ,
* Geneviève Sassolas44Unite de Soins, Centre de Médecine Nucléaire, 59 boulevard Pinel, 69003 Lyon, France,
* Bernard Schott
Cephalalgia
Volume 4 Issue 4 Page 213-220, December 1984
Although migraineurs appear in general to be hypersensitive to external stimuli, they maybe also have increased daytime sleepiness and complain of fatigue. Neurophisiological studies between attacks have shown that for a number of different sensory modalities the migrainous brain is characterised by a lack of habituation of evoked responses. Whether this is due to increased cortical hyperexcitability, possibly due to decreased inhibition, or to an abnormal responsivity of the cortex due a decreased preactivation level remains disputed. Studies using transcranial magnetic stimulation in particular have yielded contradictory results. We will review here the available data on cortical excitability obtained with different methodological approaches in patients over the migraine cycle. We will show that these data congruently indicate that the sensory cortices of migraineurs react excessively to repetitive, but not to single, stimuli and that the controversy above hyper- versus hypo-excitability is merely a semantic misunderstanding. Describing the migrainous brain as ‘hyperresponsive’ would fit most of the available data. Deciphering the precise cellular and molecular underpinnings of this hyperresponsivity remains a challenge for future research. We propose, as a working hypothesis, that a thalamo-cortical dysrhythmia might be the culprit.
Is the cerebral cortex hyperexcitable or hyperresponsive in migraine?
* G Coppola11G.B. Bietti Eye Foundation-IRCCS, Department of Neurophysiology of Vision and Neurophthalmology, ,
* F Pierelli2,32University of Rome ‘La Sapienza’ Polo Pontino—I.C.O.T., Rome and 3IRCCCS-Neuromed, Pozzilli (IS), Italy, &
* J Schoenen4,5
Comparison of the Emotional Effects of a Beta-Adrenergic Blocking Agent and a Tranquilizer
This study investigated the emotional effects of the beta-adrenergic blocking agent oxprenolol (40 mg, p.o.) and the tranquilizing agent diazepam (5 mg, p.o.) in healthy subjects under three situational conditions:an emotionally neutral control situation and two situations designed to arouse different levels of anxiety. Both oxprenolol and diazepam induced positive emotional changes only in the more strongly anxiety-arousing situation. Significant differences between oxprenolol and diazepam in inducing emotional stabilization were not demonstrable.
Gisela Erdmann, Wilhelm Janke, Sigrid Köchers, Brunhild Terschlüsen
Institut fur Psychologie, Technische Universität Berlin; Lehrstuhl fur Psychologie I, Universität Würzburg, BRD
Neuropsychobiology 1984;12:143-151 (DOI: 10.1159/000118129)
Gisela Erdmann, Wilhelm Janke, Sigrid Köchers, Brunhild Terschlüsen
Institut fur Psychologie, Technische Universität Berlin; Lehrstuhl fur Psychologie I, Universität Würzburg, BRD
Neuropsychobiology 1984;12:143-151 (DOI: 10.1159/000118129)
when sympathectomy results in excessive hypotension, vasoconstrictor drugs may be needed
High spinal anaesthesia may block the
nociceptive and haemodynamic responses to common
surgical events such as sternotomy. The extensive sym-
pathectomy provided by high spinal anaesthesia has po-
tential benefits and risks. If cardiac sympathectomy is achieved, there may be improvements in coronary per-
fusion. Stress response may be diminished. However,
when sympathectomy results in excessive hypotension, va-
soconstrictor drugs may be needed. These agents may
have detrimental effects on the coronary circulation, by-
pass grafts, and other organs.30"32
11 Parsonnet V, Dean D, Bernstein AD. A method of uni-
form stratification of risk for evaluating the results of
surgery in acquired adult heart disease. Circulation 1989;
79 (Suppl I): 13-112.
12 Robbins GR, Wynands JE, Whalley DG, et al.
nociceptive and haemodynamic responses to common
surgical events such as sternotomy. The extensive sym-
pathectomy provided by high spinal anaesthesia has po-
tential benefits and risks. If cardiac sympathectomy is achieved, there may be improvements in coronary per-
fusion. Stress response may be diminished. However,
when sympathectomy results in excessive hypotension, va-
soconstrictor drugs may be needed. These agents may
have detrimental effects on the coronary circulation, by-
pass grafts, and other organs.30"32
11 Parsonnet V, Dean D, Bernstein AD. A method of uni-
form stratification of risk for evaluating the results of
surgery in acquired adult heart disease. Circulation 1989;
79 (Suppl I): 13-112.
12 Robbins GR, Wynands JE, Whalley DG, et al.
Heart rate, heart rate variability and skin conductance as indicators of arousal
Arousal is a physiological and psychological state of being awake. It involves the activation of the reticular activating system in the brain stem, the autonomic nervous system and the endocrine system, leading to increased heart rate and blood pressure and a condition of sensory alertness, mobility and readiness to respond.
There are many different neural systems involved in what is collectively known as the arousal system. Four major systems originating in the brainstem, with connections extending throughout the cortex, are based on the brain's neurotransmitters, acetylcholine, norepinephrine, dopamine, and serotonin. When these systems are in action, the receiving neural areas become sensitive and responsive to incoming signals.
Importance
Arousal is important in regulating consciousness, attention, and information processing. It is crucial for motivating certain behaviours, such as mobility, the pursuit of nutrition, the fight or flight response and sexual activity (see Masters and Johnson's human sexual response cycle, where it is known as the arousal phase). It is also very important in emotion, and has been included as a part of many influential theories such as the James-Lange theory of emotion. According to Hans Eysenck, differences in baseline arousal level lead people to be either extraverts or introverts.
There are many different neural systems involved in what is collectively known as the arousal system. Four major systems originating in the brainstem, with connections extending throughout the cortex, are based on the brain's neurotransmitters, acetylcholine, norepinephrine, dopamine, and serotonin. When these systems are in action, the receiving neural areas become sensitive and responsive to incoming signals.
Importance
Arousal is important in regulating consciousness, attention, and information processing. It is crucial for motivating certain behaviours, such as mobility, the pursuit of nutrition, the fight or flight response and sexual activity (see Masters and Johnson's human sexual response cycle, where it is known as the arousal phase). It is also very important in emotion, and has been included as a part of many influential theories such as the James-Lange theory of emotion. According to Hans Eysenck, differences in baseline arousal level lead people to be either extraverts or introverts.
Adrenaline or peripheral noradrenaline depletion and passive avoidance in the rat
Physiol Behav. 1972 Jun;8(6):1059-62.
Adrenaline or peripheral noradrenaline depletion and passive avoidance in the rat.
Di Giusto EL.
J Comp Physiol Psychol. 1972 Dec;81(3):491-500.Links
Chemical sympathectomy and avoidance learning in the rat.
Di Giusto EL, King MG.
Adrenaline or peripheral noradrenaline depletion and passive avoidance in the rat.
Di Giusto EL.
J Comp Physiol Psychol. 1972 Dec;81(3):491-500.Links
Chemical sympathectomy and avoidance learning in the rat.
Di Giusto EL, King MG.
Heart rate and blood pressure responses to signaled and unsignaled shocks: effects of cardiac sympathectomy
J Comp Physiol Psychol. 1969 Jun;68(2):163-74.Links
Heart rate and blood pressure responses to signaled and unsignaled shocks: effects of cardiac sympathectomy.
Katcher AH, Solomon RL, Turner LH, LoLordo V, Overmier JB, Rescorla RA.
Heart rate and blood pressure responses to signaled and unsignaled shocks: effects of cardiac sympathectomy.
Katcher AH, Solomon RL, Turner LH, LoLordo V, Overmier JB, Rescorla RA.
adrenergic nerve degeneration after sympathectomy of the pineal gland
Electron microscopic evidence that bretylium and pargyline delay adrenergic nerve degeneration after sympathectomy of the pineal gland
Journal Naunyn-Schmiedeberg's Archives of Pharmacology
Publisher Springer Berlin / Heidelberg
ISSN 0028-1298 (Print) 1432-1912 (Online)
Issue Volume 319, Number 2 / May, 1982
Journal Naunyn-Schmiedeberg's Archives of Pharmacology
Publisher Springer Berlin / Heidelberg
ISSN 0028-1298 (Print) 1432-1912 (Online)
Issue Volume 319, Number 2 / May, 1982
Effects of thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis on bronchial responsiveness
Respirology. 1996 Sep;1(3):195-9.Links
Effects of thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis on bronchial responsiveness to histamine: implications on the autonomic imbalance theory of asthma.
Noppen MM, Vincken WG.
Respiratory Division, Academic Hospital AZ-VUB, Free University of Brussels, Belgium.
Three of the 26 patients (12%) without pre-operative bronchial hyperresponsiveness became hyperresponsive after TS, whereas 1 of the 9 patients with pre-operative BHR lost hyperresponsiveness. Upper dorsal thoracoscopic D2-D3 sympathicolysis performed for the treatment of EH has no significant effects on mean PD20 His and individual loss (11%) or development (12%) of BHR occurs only in 12% of patients.
Effects of thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis on bronchial responsiveness to histamine: implications on the autonomic imbalance theory of asthma.
Noppen MM, Vincken WG.
Respiratory Division, Academic Hospital AZ-VUB, Free University of Brussels, Belgium.
Three of the 26 patients (12%) without pre-operative bronchial hyperresponsiveness became hyperresponsive after TS, whereas 1 of the 9 patients with pre-operative BHR lost hyperresponsiveness. Upper dorsal thoracoscopic D2-D3 sympathicolysis performed for the treatment of EH has no significant effects on mean PD20 His and individual loss (11%) or development (12%) of BHR occurs only in 12% of patients.
beta 1-adrenoreceptor-mediated change in pulmonary capillary membrane permeability
Respir Med. 1997 Oct;91(9):537-45.Click here to read Links
Partial pulmonary sympathetic denervation by thoracoscopic D2-D3 sympathicolysis for essential hyperhidrosis: effect on the pulmonary diffusion capacity.
Noppen MM, Vincken WG.
Respiratory Division, Academic Hospital, University of Brussels, Belgium.
In patients with essential hyperhidrosis (EH), a pathological condition characterized by increased activity of the upper dorsal sympathetic ganglia D2-D3, anatomical interruption at the D2-D3 level by thoracoscopic sympathicolysis (TS) is a safe and effective treatment. The D2 and D3 ganglia, however, are also in the pathway of sympathetic lung innervation, which may influence the pulmonary diffusion capacity for carbon monoxide (expressed as transfer factor for CO:TLCO, and as transfer coefficient for CO:KCO). We therefore studied the effect of TS on TLCO and KCO in 50 EH patients: compared with pre-operative values, both TLCO (-6.7%, P < 0.001) and KCO (-4.2%, P = 0.002) were significantly decreased at 6 weeks after bilateral TS, an effect which was independent of the smoking status of the patients. In order to explain this phenomenon, the following pharmacological interventions were studied: (1) oral beta 1 + 2-adrenoreceptor blockade with propranolol caused a comparable decrease of TLCO (-6.3%) and KCO (-7.5%) in matched normal subjects, but had no effect on TLCO and KCO in EH patients prior to TS; and (2) subsequent inhalation of the beta 2-adrenoreceptor agonist salbutamol in a dosage suspected to cause alveolar beta-receptor stimulation had no effect on TLCO and KCO, neither in the normal subjects, nor in EH patients (before and after TS). Although the exact mechanism of the TS-induced decrease in TLCO and KCO remains speculative, these findings suggest that they may be related to a beta 1-adrenoreceptor-mediated change in pulmonary capillary membrane permeability, although TS-induced changes in pulmonary blood flow or an interplay of both mechanisms cannot be excluded.
Partial pulmonary sympathetic denervation by thoracoscopic D2-D3 sympathicolysis for essential hyperhidrosis: effect on the pulmonary diffusion capacity.
Noppen MM, Vincken WG.
Respiratory Division, Academic Hospital, University of Brussels, Belgium.
In patients with essential hyperhidrosis (EH), a pathological condition characterized by increased activity of the upper dorsal sympathetic ganglia D2-D3, anatomical interruption at the D2-D3 level by thoracoscopic sympathicolysis (TS) is a safe and effective treatment. The D2 and D3 ganglia, however, are also in the pathway of sympathetic lung innervation, which may influence the pulmonary diffusion capacity for carbon monoxide (expressed as transfer factor for CO:TLCO, and as transfer coefficient for CO:KCO). We therefore studied the effect of TS on TLCO and KCO in 50 EH patients: compared with pre-operative values, both TLCO (-6.7%, P < 0.001) and KCO (-4.2%, P = 0.002) were significantly decreased at 6 weeks after bilateral TS, an effect which was independent of the smoking status of the patients. In order to explain this phenomenon, the following pharmacological interventions were studied: (1) oral beta 1 + 2-adrenoreceptor blockade with propranolol caused a comparable decrease of TLCO (-6.3%) and KCO (-7.5%) in matched normal subjects, but had no effect on TLCO and KCO in EH patients prior to TS; and (2) subsequent inhalation of the beta 2-adrenoreceptor agonist salbutamol in a dosage suspected to cause alveolar beta-receptor stimulation had no effect on TLCO and KCO, neither in the normal subjects, nor in EH patients (before and after TS). Although the exact mechanism of the TS-induced decrease in TLCO and KCO remains speculative, these findings suggest that they may be related to a beta 1-adrenoreceptor-mediated change in pulmonary capillary membrane permeability, although TS-induced changes in pulmonary blood flow or an interplay of both mechanisms cannot be excluded.
Wednesday, April 30, 2008
the cardiovascular and pulmonary effects that are observed after TS may be associated with the decrease in NA
Eur J Clin Invest. 1997 Mar;27(3):202-5.Links
Plasma catecholamine concentrations in essential hyperhidrosis and effects of thoracoscopic D2-D3 sympathicolysis.
Noppen M, Sevens C, Gerlo E, Vincken W.
Respiratory Division, Academic Hospital AZ-VUB, Free University of Brussels, Belgium.
Essential hyperhidrosis (EH) is caused by a poorly understood overactivity of the sympathetic fibres passing through the upper dorsal sympathetic ganglia D2 and D3. These ganglia are also in the pathway of the sympathetic innervation of the heart and lungs. Therefore, although the predominant sympathetic neurotransmitter at the eccrine sweat glands is acetylcholine, the plasma concentration of noradrenaline (NA) (which is the main sympathetic neurotransmitter at the end organs including the heart and the lungs) may be elevated. Furthermore, as there are some indications for generalized sympathetic overactivity in EH, the plasma concentration of adrenaline (A) may also be elevated. Plasma levels of NA and A were therefore determined in 13 EH patients before and after thoracoscopic D2-D3 sympathicolysis (TS). Preoperative NA and A plasma levels were all within the normal limits used in our laboratory. After TS, mean NA plasma levels are significantly decreased, whereas mean A are unchanged. We conclude that sympathetic overactivity in EH is limited to the upper dorsal sympathetic ganglia and that some of the cardiovascular and pulmonary effects that are observed after TS may be associated with the decrease in NA.
Plasma catecholamine concentrations in essential hyperhidrosis and effects of thoracoscopic D2-D3 sympathicolysis.
Noppen M, Sevens C, Gerlo E, Vincken W.
Respiratory Division, Academic Hospital AZ-VUB, Free University of Brussels, Belgium.
Essential hyperhidrosis (EH) is caused by a poorly understood overactivity of the sympathetic fibres passing through the upper dorsal sympathetic ganglia D2 and D3. These ganglia are also in the pathway of the sympathetic innervation of the heart and lungs. Therefore, although the predominant sympathetic neurotransmitter at the eccrine sweat glands is acetylcholine, the plasma concentration of noradrenaline (NA) (which is the main sympathetic neurotransmitter at the end organs including the heart and the lungs) may be elevated. Furthermore, as there are some indications for generalized sympathetic overactivity in EH, the plasma concentration of adrenaline (A) may also be elevated. Plasma levels of NA and A were therefore determined in 13 EH patients before and after thoracoscopic D2-D3 sympathicolysis (TS). Preoperative NA and A plasma levels were all within the normal limits used in our laboratory. After TS, mean NA plasma levels are significantly decreased, whereas mean A are unchanged. We conclude that sympathetic overactivity in EH is limited to the upper dorsal sympathetic ganglia and that some of the cardiovascular and pulmonary effects that are observed after TS may be associated with the decrease in NA.
Endoscopic thoracic sympathectomy suppresses baroreflex control of heart rate in patients with essential hyperhidrosis
J Anesth. 2002;16(1):3.Click here to read Links
Comment on:
J Anesth. 2002;16(1):4-8.
The effect of thoracic sympathectomy on baroreflex control of circulation.
Hoka S
Anesth Analg. 2004 Jan;98(1):37-9, table of contents.Click here to read Links
Endoscopic thoracic sympathectomy suppresses baroreflex control of heart rate in patients with essential hyperhidrosis.
Kawamata YT, Kawamata T, Omote K, Homma E, Hanzawa T, Kaneko T, Namiki A.
Department of Anesthesiology, Nippon Telegraph and Telephone East Japan Sapporo Hospital, Sapporo, Japan.
Endoscopic thoracic (T2-3 or T3-4) sympathectomy (ETS) is a highly effective treatment for palmar hyperhidrosis. Because the T2-3 or T3-4 sympathetic ganglia are involved in direct sympathetic innervation of the heart, sympathectomy at this level may alter baroreflex control of heart rate. The purpose of our study was to examine the influence of ETS on baroreflex responses to pressor and depressor stimuli under small-dose sevoflurane anesthesia. We studied 40 patients with palmar or axillary hyperhidrosis who were scheduled to receive ETS. In the ETS procedure, the sympathetic trunk was identified by using thoracic endoscopy and was transected. Before and after ETS, the pressor or depressor test was performed by using an IV infusion of phenylephrine or nitroglycerin, respectively, under small-dose general anesthesia. Baroreflex sensitivity was calculated from R-R intervals and systolic blood pressure. ETS did not change heart rate and systemic blood pressure at rest, although ETS significantly altered baroreflex in both pressor and depressor tests in all patients. Baroreflex was completely suppressed in 1 of 19 patients in the pressor test and in 9 of 21 patients in the depressor test. We conclude that baroreflex responses are suppressed in patients who receive ETS. IMPLICATIONS: Endoscopic thoracic sympathectomy suppressed the baroreflex control of heart rate during pressor and depressor tests in patients with palmar or axillary hyperhidrosis.
Thoracoscopic D2-D3 sympathicolysis has a partial beta-blocker-like activity, which results in a decrease in heart rate at rest and during maximal exercise, and in the diastolic blood pressure response to the handgrip test. Further studies are needed to assess the long-term consequences of this procedure.
J Auton Nerv Syst. 1996 Sep 12;60(3):115-20.Click here to read Links
Changes in cardiocirculatory autonomic function after thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis.
Noppen M, Dendale P, Hagers Y, Herregodts P, Vincken W, D'Haens J.
Respiratory Department of the University Hospital AZ-VUB, Free University, Brussels, Belgium.
Comment on:
J Anesth. 2002;16(1):4-8.
The effect of thoracic sympathectomy on baroreflex control of circulation.
Hoka S
Anesth Analg. 2004 Jan;98(1):37-9, table of contents.Click here to read Links
Endoscopic thoracic sympathectomy suppresses baroreflex control of heart rate in patients with essential hyperhidrosis.
Kawamata YT, Kawamata T, Omote K, Homma E, Hanzawa T, Kaneko T, Namiki A.
Department of Anesthesiology, Nippon Telegraph and Telephone East Japan Sapporo Hospital, Sapporo, Japan.
Endoscopic thoracic (T2-3 or T3-4) sympathectomy (ETS) is a highly effective treatment for palmar hyperhidrosis. Because the T2-3 or T3-4 sympathetic ganglia are involved in direct sympathetic innervation of the heart, sympathectomy at this level may alter baroreflex control of heart rate. The purpose of our study was to examine the influence of ETS on baroreflex responses to pressor and depressor stimuli under small-dose sevoflurane anesthesia. We studied 40 patients with palmar or axillary hyperhidrosis who were scheduled to receive ETS. In the ETS procedure, the sympathetic trunk was identified by using thoracic endoscopy and was transected. Before and after ETS, the pressor or depressor test was performed by using an IV infusion of phenylephrine or nitroglycerin, respectively, under small-dose general anesthesia. Baroreflex sensitivity was calculated from R-R intervals and systolic blood pressure. ETS did not change heart rate and systemic blood pressure at rest, although ETS significantly altered baroreflex in both pressor and depressor tests in all patients. Baroreflex was completely suppressed in 1 of 19 patients in the pressor test and in 9 of 21 patients in the depressor test. We conclude that baroreflex responses are suppressed in patients who receive ETS. IMPLICATIONS: Endoscopic thoracic sympathectomy suppressed the baroreflex control of heart rate during pressor and depressor tests in patients with palmar or axillary hyperhidrosis.
Thoracoscopic D2-D3 sympathicolysis has a partial beta-blocker-like activity, which results in a decrease in heart rate at rest and during maximal exercise, and in the diastolic blood pressure response to the handgrip test. Further studies are needed to assess the long-term consequences of this procedure.
J Auton Nerv Syst. 1996 Sep 12;60(3):115-20.Click here to read Links
Changes in cardiocirculatory autonomic function after thoracoscopic upper dorsal sympathicolysis for essential hyperhidrosis.
Noppen M, Dendale P, Hagers Y, Herregodts P, Vincken W, D'Haens J.
Respiratory Department of the University Hospital AZ-VUB, Free University, Brussels, Belgium.
ARE WE PAYING A HIGH PRICE FOR SYMPATHECTOMY?
www.spinalinjection.com/pdf/newsletters/Summer2001.pdf
A Systematic Literature Review of Late Complications
Conclusions: Surgical sympathectomy irrespective of approach is accompanied by several potentially
disabling complications.
Andrea Furlan
MD, Angela Mailis
MD, MSc, FRCPC (PhysMed) and
Marios Papagapiou
MSc
Comprehensive Pain Program
and Toronto Western Hospital Research Institute
The Toronto Western Hospital, and Institute for Work & Health
, Toronto, Ontario,
Canada.
A Systematic Literature Review of Late Complications
Conclusions: Surgical sympathectomy irrespective of approach is accompanied by several potentially
disabling complications.
Andrea Furlan
MD, Angela Mailis
MD, MSc, FRCPC (PhysMed) and
Marios Papagapiou
MSc
Comprehensive Pain Program
and Toronto Western Hospital Research Institute
The Toronto Western Hospital, and Institute for Work & Health
, Toronto, Ontario,
Canada.
Regeneration after cervicothoracic sympathectomy producing gustatory responses.
Angiology. 1966 Mar;17(3):143-7.Links
Regeneration after cervicothoracic sympathectomy producing gustatory responses.
Bloor K.
http://www.ncbi.nlm.nih.gov/pubmed/5909808
Gustatory sweating demonstrated by infrared thermography]
[Article in German]
Plendl H, Paulus W, Witt TN.
Neurologische Klinik, Klinikum Grosshadern, Universität München.
The hypaesthesia improved, but the sympathetic nerve deficits remained. There were no other neurological signs. 9 months later, within one minute of eating a sour apple, the patient developed severe sweating over the left half of the face and the left chest. The reaction was confirmed by infra-red thermography which proved that the skin temperature in the sweating region had fallen to 3 degrees C. The likely cause of localized gustatory sweating is intra-operative damage of the stellate ganglion or its preganglionic nerve connections. Treatment is limited to avoidance of the precipitating gustatory stimulus.
Dtsch Med Wochenschr. 1992 Oct 9;117(41):1556-60.
Application of medical thermography to the diagnosis of Frey's syndrome.
Isogai N, Kamiishi H.
Department of Plastic and Reconstructive Surgery, Kinki University Hospital, Osaka, Japan.
BACKGROUND: In Frey's syndrome, the secretory parasympathetic fibers of the parotid gland are thought to communicate with the sympathetic nerve fibers of sweat glands and blood vessels of the skin following parotidectomy. Miscommunication results in subjective gustatory sweating and facial flushing, which appear early with postoperative mastication. In this study, we compared the efficacy of medical thermography to the Minor's starch-iodine test to determine the presence of gustatory sweating in Frey's syndrome. METHODS: Patients were considered to have Frey's syndrome if signs of gustatory sweating and localized skin flushing of the parotid region were present. In four patients who had undergone unilateral parotidectomy, gustatory sweating and facial flushing were present after gustatory stimulation, and the presence of Frey's syndrome was confirmed with Minor's starch test in all patients. Infrared thermography was then performed, and the same area measured. The contralateral side served as an internal control for each patient. RESULTS: Before gustatory stimulation, the isothermal pattern of the diseased side and the nonoperative side was similar. Stress thermography using a sialogogue (lemon, 3 mL) showed a cold spot at the operative site in all four patients with Frey's syndrome. The contralateral nonoperative side showed normal skin temperature distribution in all patients. Minor's test was positive in all patients. CONCLUSIONS: Thermography is a noninvasive, facile test that provides a qualitative visual analysis of the cutaneous capillary response in Frey's syndrome following parotid surgery.
Regeneration after cervicothoracic sympathectomy producing gustatory responses.
Bloor K.
http://www.ncbi.nlm.nih.gov/pubmed/5909808
Gustatory sweating demonstrated by infrared thermography]
[Article in German]
Plendl H, Paulus W, Witt TN.
Neurologische Klinik, Klinikum Grosshadern, Universität München.
The hypaesthesia improved, but the sympathetic nerve deficits remained. There were no other neurological signs. 9 months later, within one minute of eating a sour apple, the patient developed severe sweating over the left half of the face and the left chest. The reaction was confirmed by infra-red thermography which proved that the skin temperature in the sweating region had fallen to 3 degrees C. The likely cause of localized gustatory sweating is intra-operative damage of the stellate ganglion or its preganglionic nerve connections. Treatment is limited to avoidance of the precipitating gustatory stimulus.
Dtsch Med Wochenschr. 1992 Oct 9;117(41):1556-60.
Application of medical thermography to the diagnosis of Frey's syndrome.
Isogai N, Kamiishi H.
Department of Plastic and Reconstructive Surgery, Kinki University Hospital, Osaka, Japan.
BACKGROUND: In Frey's syndrome, the secretory parasympathetic fibers of the parotid gland are thought to communicate with the sympathetic nerve fibers of sweat glands and blood vessels of the skin following parotidectomy. Miscommunication results in subjective gustatory sweating and facial flushing, which appear early with postoperative mastication. In this study, we compared the efficacy of medical thermography to the Minor's starch-iodine test to determine the presence of gustatory sweating in Frey's syndrome. METHODS: Patients were considered to have Frey's syndrome if signs of gustatory sweating and localized skin flushing of the parotid region were present. In four patients who had undergone unilateral parotidectomy, gustatory sweating and facial flushing were present after gustatory stimulation, and the presence of Frey's syndrome was confirmed with Minor's starch test in all patients. Infrared thermography was then performed, and the same area measured. The contralateral side served as an internal control for each patient. RESULTS: Before gustatory stimulation, the isothermal pattern of the diseased side and the nonoperative side was similar. Stress thermography using a sialogogue (lemon, 3 mL) showed a cold spot at the operative site in all four patients with Frey's syndrome. The contralateral nonoperative side showed normal skin temperature distribution in all patients. Minor's test was positive in all patients. CONCLUSIONS: Thermography is a noninvasive, facile test that provides a qualitative visual analysis of the cutaneous capillary response in Frey's syndrome following parotid surgery.
Sympathetic ingrowth retards recovery processes.
Sympathetic sprouting and recovery of a spatial behavior.
Harrell LE, Barlow TS, Davis JN.
After lesions of the medial septum, peripheral sympathetic fibers from the superior cervical ganglion appear in the hippocampal formation. To assess the functional significance of this neuronal rearrangement, we analyzed behavior on a spatial/memory task sensitive to hippocampal dysfunction, the radial eight-arm maze. The procedure allowed evaluation of both working and reference memory. All rats were able to master the task. Half of the rats then underwent either medial septal lesions and ganglionectomy or sham neurosurgery and ganglionectomy, and the other half underwent medial septal lesions or sham neurosurgery followed by ganglionectomy after further behavioral testing. Medial septal lesions in both groups disrupted taks performance with recovery of performance occurring with time. However, the rate of recovery was significantly enhanced in rats which had septal lesions and ganglionectomies simultaneously. Removal of the ganglion after recovery produced no effects on maze performance. Our results suggest that sympathetic ingrowth retards recovery processes.
Exp Neurol. 1983 Nov;82(2):379-90
http://www.ncbi.nlm.nih.gov/pubmed/6628625
Harrell LE, Barlow TS, Davis JN.
After lesions of the medial septum, peripheral sympathetic fibers from the superior cervical ganglion appear in the hippocampal formation. To assess the functional significance of this neuronal rearrangement, we analyzed behavior on a spatial/memory task sensitive to hippocampal dysfunction, the radial eight-arm maze. The procedure allowed evaluation of both working and reference memory. All rats were able to master the task. Half of the rats then underwent either medial septal lesions and ganglionectomy or sham neurosurgery and ganglionectomy, and the other half underwent medial septal lesions or sham neurosurgery followed by ganglionectomy after further behavioral testing. Medial septal lesions in both groups disrupted taks performance with recovery of performance occurring with time. However, the rate of recovery was significantly enhanced in rats which had septal lesions and ganglionectomies simultaneously. Removal of the ganglion after recovery produced no effects on maze performance. Our results suggest that sympathetic ingrowth retards recovery processes.
Exp Neurol. 1983 Nov;82(2):379-90
http://www.ncbi.nlm.nih.gov/pubmed/6628625
Leptin Affects Pancreatic Endocrine Functions through
AKIRA MIZUNO†, TAKASHI MURAKAMI†, SHIZUKA OTANI,
MASAMICHI KUWAJIMA, AND KENJI SHIMA
Department of Laboratory Medicine, School of Medicine, the University of Tokushima, Tokushima
770-8503, Japan
ABSTRACT
The effects of leptin on the secretion of insulin and glucagon were
examined. In an experiment involving insulin response to an iv glu-
cose load in vagotomized rats, the plasma concentrations of insulin
were significantly lower in the leptin (20 nmol/kg BW)-treated group
than in a control group. However, in intact rats and rats that had
undergone both vagotomy and chemical sympathectomy, this sup-
pressive effect of leptin on insulin secretion was not detected. In an
experiment involving a hypoglycemia-induced glucagon secretion test
in intact rats, an iv injection of leptin (20 nmol/kg BW) augmented the
plasma glucagon response to hypoglycemia. In the case of sympa-
thectomized rats, however, this stimulative effect of leptin on gluca-
gon secretion was not detected. In an experiment with perfused rat
pancreas, the addition of leptin (20 nM) to the perfusate slightly
suppressed insulin secretion, but had no effect on basal or glucopenia-
induced glucagon secretion. In intact rats infused with leptin (0.31
MASAMICHI KUWAJIMA, AND KENJI SHIMA
Department of Laboratory Medicine, School of Medicine, the University of Tokushima, Tokushima
770-8503, Japan
ABSTRACT
The effects of leptin on the secretion of insulin and glucagon were
examined. In an experiment involving insulin response to an iv glu-
cose load in vagotomized rats, the plasma concentrations of insulin
were significantly lower in the leptin (20 nmol/kg BW)-treated group
than in a control group. However, in intact rats and rats that had
undergone both vagotomy and chemical sympathectomy, this sup-
pressive effect of leptin on insulin secretion was not detected. In an
experiment involving a hypoglycemia-induced glucagon secretion test
in intact rats, an iv injection of leptin (20 nmol/kg BW) augmented the
plasma glucagon response to hypoglycemia. In the case of sympa-
thectomized rats, however, this stimulative effect of leptin on gluca-
gon secretion was not detected. In an experiment with perfused rat
pancreas, the addition of leptin (20 nM) to the perfusate slightly
suppressed insulin secretion, but had no effect on basal or glucopenia-
induced glucagon secretion. In intact rats infused with leptin (0.31
plasma concentration of glucose that signals the need by the central nervous system to mobilize energy reserves depends on a number of factors
Greenspan's Basic and Clinical Endocrinology, 8th Ed.
Pathophysiology of the Counterregulatory Response to Neuroglycopenia
Sections: Pathophysiology of the Counterregulatory Response to Neuroglycopenia, Counterregulatory Response to Hypoglycemia, Insulin, Catecholamines, Glucagon, Corticotropin and Hydrocortisone, Growth Hormone, Cholinergic Neurotransmitters, Maintenance of Euglycemia in the Postabsorptive State, Role of the Kidney, Role of PGC-1 in Regulation of Gluconeogenesis.
Topics Discussed: acetylcholine; catecholamines; corticotropin; glucagon; gluconeogenesis; hydrocortisone; hypoglycemia; insulin; kidney; liver; neuroglycopenia; somatotropin.
Excerpt: "The plasma concentration of glucose that signals the need by the central nervous system to mobilize energy reserves depends on a number of factors, such as the status of blood flow to the brain, the integrity of cerebral tissue, the prevailing arterial level of plasma glucose, the rapidity with which plasma glucose concentration falls, and the availability of alternative metabolic fuels.Endogenous insulin secretion is lowered both by reduced glucose stimulation to the pancreatic cell and by sympathetic nervous system inhibition from a combination of alpha-adrenergic neural effects and increased circulating catecholamine levels. This reactive insulinopenia appears to be essential for glucose recovery, because it facilitates the mobilization of energy from existing energy stores (glycogenolysis and lipolysis); increases hepatic enzymes involved in gluconeogenesis and ketogenesis; increases enzymes of the renal cortex, promoting gluconeogenesis; and at the same time prevents muscle tissue from consuming the blood glucose being released from the liver (Chapter 18)...."
Pathophysiology of the Counterregulatory Response to Neuroglycopenia
Sections: Pathophysiology of the Counterregulatory Response to Neuroglycopenia, Counterregulatory Response to Hypoglycemia, Insulin, Catecholamines, Glucagon, Corticotropin and Hydrocortisone, Growth Hormone, Cholinergic Neurotransmitters, Maintenance of Euglycemia in the Postabsorptive State, Role of the Kidney, Role of PGC-1 in Regulation of Gluconeogenesis.
Topics Discussed: acetylcholine; catecholamines; corticotropin; glucagon; gluconeogenesis; hydrocortisone; hypoglycemia; insulin; kidney; liver; neuroglycopenia; somatotropin.
Excerpt: "The plasma concentration of glucose that signals the need by the central nervous system to mobilize energy reserves depends on a number of factors, such as the status of blood flow to the brain, the integrity of cerebral tissue, the prevailing arterial level of plasma glucose, the rapidity with which plasma glucose concentration falls, and the availability of alternative metabolic fuels.Endogenous insulin secretion is lowered both by reduced glucose stimulation to the pancreatic cell and by sympathetic nervous system inhibition from a combination of alpha-adrenergic neural effects and increased circulating catecholamine levels. This reactive insulinopenia appears to be essential for glucose recovery, because it facilitates the mobilization of energy from existing energy stores (glycogenolysis and lipolysis); increases hepatic enzymes involved in gluconeogenesis and ketogenesis; increases enzymes of the renal cortex, promoting gluconeogenesis; and at the same time prevents muscle tissue from consuming the blood glucose being released from the liver (Chapter 18)...."
Chemical sympathectomy resulted in a highly significant increase in acid and pepsin secretion.
The effect of chemical sympathectomy on insulin-stimulated gastric secretion in dogs.
Grabner P, Holian O, Kalahanis NG, Torma Grabner E, Bombeck CT, Nyhus LM.
Administration of 6 hydroxydopamine (6 OHDA) causes selective acute degeneration of the adrenergic nerve terminals, that is a reversible chemical sympathectomy. The effect of this drug was studied on the insulin stimulated gastric secretion. Insulin stimulated (0.15-0.4 IU/kg) gastric acid and pepsin output and serum gastrin was measured before and after 6 OHDA treatment (40 mg/kg) in gastric fistula dogs. Chemical sympathectomy resulted in a highly significant increase in acid and pepsin secretion. However, the hypoglycemic gastrin release was unaltered except the peak response, which showed a significant reduction. These data confirm earlier observations, that the sympathetic innervation of the stomach has an inhibitory effect on gastric secretion in the dog. Furthermore it seems that the adrenergic fibres in the vagus nerve might have some moduling effect on the insulin induced gastrin release.
Scand J Gastroenterol Suppl. 1984;89:95-8
http://www.ncbi.nlm.nih.gov/pubmed/6429840
Grabner P, Holian O, Kalahanis NG, Torma Grabner E, Bombeck CT, Nyhus LM.
Administration of 6 hydroxydopamine (6 OHDA) causes selective acute degeneration of the adrenergic nerve terminals, that is a reversible chemical sympathectomy. The effect of this drug was studied on the insulin stimulated gastric secretion. Insulin stimulated (0.15-0.4 IU/kg) gastric acid and pepsin output and serum gastrin was measured before and after 6 OHDA treatment (40 mg/kg) in gastric fistula dogs. Chemical sympathectomy resulted in a highly significant increase in acid and pepsin secretion. However, the hypoglycemic gastrin release was unaltered except the peak response, which showed a significant reduction. These data confirm earlier observations, that the sympathetic innervation of the stomach has an inhibitory effect on gastric secretion in the dog. Furthermore it seems that the adrenergic fibres in the vagus nerve might have some moduling effect on the insulin induced gastrin release.
Scand J Gastroenterol Suppl. 1984;89:95-8
http://www.ncbi.nlm.nih.gov/pubmed/6429840
hypoglycemia have also been found in patients following sympathectomy
Diseases of the Motor System - Google Books Result
by Pierre J. Vinken, G. W. Bruyn, Harold L. Klawans, J. M. B. V. de Jong - 1991 - Medical - 529 pages
Hypoglycemia induced by insulin is a potent stimulus for epinephrine secretion. ... hypoglycemia have also been found in patients following sympathectomy. ...
books.google.com.au/books?isbn=0444812784...
by Pierre J. Vinken, G. W. Bruyn, Harold L. Klawans, J. M. B. V. de Jong - 1991 - Medical - 529 pages
Hypoglycemia induced by insulin is a potent stimulus for epinephrine secretion. ... hypoglycemia have also been found in patients following sympathectomy. ...
books.google.com.au/books?isbn=0444812784...
Adrenal tyrosine hydroxylase: compensatory increase in activity after chemical sympathectomy
Mueller RA, Thoenen H, Axelrod J.
Destruction of peripheral sympathetic nerve endings with 6-hydroxydopamine causes a disappearance of cardiac tyrosine hydroxylase, accompanied by a twofold increase in adrenal tyrosine hydroxylase and a small increase in phenyl-ethanolanine-N-methyl transferase. No change in adrenal catecholamine content occurs under these conditions.
Science. 1969 Jan 31;163(866):468-9
http://www.ncbi.nlm.nih.gov/pubmed/5762395
Destruction of peripheral sympathetic nerve endings with 6-hydroxydopamine causes a disappearance of cardiac tyrosine hydroxylase, accompanied by a twofold increase in adrenal tyrosine hydroxylase and a small increase in phenyl-ethanolanine-N-methyl transferase. No change in adrenal catecholamine content occurs under these conditions.
Science. 1969 Jan 31;163(866):468-9
http://www.ncbi.nlm.nih.gov/pubmed/5762395
Sympathectomy for Inner-Ear Vascular Insufficiency
The Journal of Laryngology & Otology (1960), 74:951-970 Cambridge University Press
Copyright © JLO (1984) Limited 1960
doi:10.1017/S0022215100057388
Research Article
Observations on Sympathectomy in the Treatment of Ménière's Disease
Philip H. Golding-Wooda1
a1 “Oakleigh”, 19 The Landway, Bearsted, Maidstone, Kent
Rev Bras Otorinolaringol. 1952 Mar-Apr;20(2):31-40.Links
[Results of sympathectomy in 110 cases of Menière's disease.]
[Article in Undetermined Language]
PASSE EG.
Arch Otolaryngol. 1973 May;97(5):391-4.Links
Cervical sympathectomy in Meniere's disease.
Golding-Wood PH.
The Journal of Laryngology & Otology (1961), 75:259-267 Cambridge University Press
Copyright © JLO (1984) Limited 1961
doi:10.1017/S002221510005773X
Research Article
Sympathectomy for Inner-Ear Vascular Insufficiency
T. J. Wilmota1
a1 Tyrone County Hospital, Omagh, Co. Tyrone, Northern Ireland
Article author query
wilmot tj [PubMed] [Google Scholar]
Copyright © JLO (1984) Limited 1960
doi:10.1017/S0022215100057388
Research Article
Observations on Sympathectomy in the Treatment of Ménière's Disease
Philip H. Golding-Wooda1
a1 “Oakleigh”, 19 The Landway, Bearsted, Maidstone, Kent
Rev Bras Otorinolaringol. 1952 Mar-Apr;20(2):31-40.Links
[Results of sympathectomy in 110 cases of Menière's disease.]
[Article in Undetermined Language]
PASSE EG.
Arch Otolaryngol. 1973 May;97(5):391-4.Links
Cervical sympathectomy in Meniere's disease.
Golding-Wood PH.
The Journal of Laryngology & Otology (1961), 75:259-267 Cambridge University Press
Copyright © JLO (1984) Limited 1961
doi:10.1017/S002221510005773X
Research Article
Sympathectomy for Inner-Ear Vascular Insufficiency
T. J. Wilmota1
a1 Tyrone County Hospital, Omagh, Co. Tyrone, Northern Ireland
Article author query
wilmot tj [PubMed] [Google Scholar]
Ultrastructural changes in the nerves innervating the cerebral artery after sympathectomy
The ultrastructure of the innervation of the anterior cerebral artery of the rat was studied in control animals and in animals after superior cervical ganglionectomy.
Fluorescence histochemistry shows a periarterial network of intensely fluorescent fibers which are divided into two groups, adventitial and periadventitial. The fluorescence begins to decrease 26 hours after, and completely disappears about 32 hours after, ganglionectomy.
Fine structural changes are first observed 18 hours after ganglionectomy, when the axoplasm of degenerating axons becomes electron dense. This density gradually increases up to about 32 hours. By 32 hours most axons with disintegrating axolemmas become inclusion bodies of the Schwann cells. At this stage, synaptic vesicles can still be distinguished as less dense areas, but the membrane structures of synaptic vesicles and mitochondria are difficult to recognize. The degenerating axons are gradually absorbed and by 38 hours dense, residual bodies are observed in the Schwann cells. Generally speaking, the degeneration occurs first in the adventitial fibers and then in the periadventitial fibers. The transient appearance of small, granular vesicles is noticed in axon terminals about 18 hours after denervation, although very few small, granular vesicles are seen in control tissue or at later stages of degeneration.
Takashi Iwayama1
(1) Department of Anatomy, Faculty of Medicine, Kyushu University, Fukuoka, Japan
Received: 22 June 1970
Ultrastructural changes in the nerves innervating the cerebral artery after sympathectomy
Journal Cell and Tissue Research
Issue Volume 109, Number 4 / December, 1970
Fluorescence histochemistry shows a periarterial network of intensely fluorescent fibers which are divided into two groups, adventitial and periadventitial. The fluorescence begins to decrease 26 hours after, and completely disappears about 32 hours after, ganglionectomy.
Fine structural changes are first observed 18 hours after ganglionectomy, when the axoplasm of degenerating axons becomes electron dense. This density gradually increases up to about 32 hours. By 32 hours most axons with disintegrating axolemmas become inclusion bodies of the Schwann cells. At this stage, synaptic vesicles can still be distinguished as less dense areas, but the membrane structures of synaptic vesicles and mitochondria are difficult to recognize. The degenerating axons are gradually absorbed and by 38 hours dense, residual bodies are observed in the Schwann cells. Generally speaking, the degeneration occurs first in the adventitial fibers and then in the periadventitial fibers. The transient appearance of small, granular vesicles is noticed in axon terminals about 18 hours after denervation, although very few small, granular vesicles are seen in control tissue or at later stages of degeneration.
Takashi Iwayama1
(1) Department of Anatomy, Faculty of Medicine, Kyushu University, Fukuoka, Japan
Received: 22 June 1970
Ultrastructural changes in the nerves innervating the cerebral artery after sympathectomy
Journal Cell and Tissue Research
Issue Volume 109, Number 4 / December, 1970
Functional and organic vascular wall changes after sympathectomy and partial nerve damage
http://www.ncbi.nlm.nih.gov/pubmed/14443457
induces a selective dopaminergic sympathectomy that simulates ideopathic Parkinson's disease
MPTP
MPTP (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine) a chemical which induces a selective dopaminergic sympathectomy that simulates ideopathic Parkinson's disease is the product of an innacurate attempted synthesis of MPPP (1-methyl-4-phenyl-4-propionoxypiperidine) from MPHP (1-methyl-4-phenyl-4-hydroxypiperide) - these are meperidine (Demerol) analoges and not amphetamine derivatives.
In 1983 a group of heroin users attempted a demerol synthesis and obtained instead a compound called MPTP. The product had a similar appearance and melting point, and they injected it expecting a demerol high. In the brain, MPTP decomposes to MPP+ which selectively bonds to and destroys dopamine receptors. These individuals thus prematurely gave themselves Parkinson's disease. MPP+ closely resembles paraquat, a defoliant used by the US government, outside US borders, against marijuana (a bit heavy handed and reckless).
In order to understand the development and behavior of central dopaminergic neurons and molecular mechanisms involved in the degeneration of such neurons in PD and MPTP-induced PD, several investigators have developed an immortalized dopaminergic cell line. The cell line is called MES 23.5 and is derived by fusion of rat embryonic mesencephalon cells with murine N18TG2 neuroblastoma cells. The cell line expresses a complex range of neural properties found in the dopaminergic neurons of the substantia nigra (Crawford et al, 1992), including tyrosine hydroxylase, dopamine synthesis, and conotoxin receptors (control of calcium channels). Only dopamine, and no other catecholamine, is synthesized by the cells. Levels of tyrosine and dopamine are elevated by 3-7 fold with the treatment of dibutyrl-cAMP. This cell line offers several advantages over other cell lines including greater homogeneity (providing more obvious and consistent observations), and susceptibility to both free radical-mediated cytotoxicity and calcium-dependent cell death.
It has been recently proposed that cerebrospinal fluid (CSF) from PD patients may possess substances which are neurotoxic for dopaminergic cells (Klawans et al, 1993; Hao et al, 1995). To define the selectivity, specificity, and property of these cytotoxic factors, investigators have employed MES 23.5 cell cultures to examine cytotoxicity of CSF from PD and non-PD patients. Preliminary studies from 5 of 7 CSF samples from PD patients, but none of 5 CSF samples from control subjects, have shown significant cytotoxic effects on MES 23.5 cells as determined by cell viability assays. The damaged cells demonstrate a pattern of apoptotic morphology including nuclear chromatin condensation and nuclear fragmentation. An approach to identify the cytotoxic factors is underway. These results raise intriguing possibilities for the etiology and pathogenesis of PD.
http://www.namiscc.org/Research/2002/Psychosis.htm
MPTP (1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine) a chemical which induces a selective dopaminergic sympathectomy that simulates ideopathic Parkinson's disease is the product of an innacurate attempted synthesis of MPPP (1-methyl-4-phenyl-4-propionoxypiperidine) from MPHP (1-methyl-4-phenyl-4-hydroxypiperide) - these are meperidine (Demerol) analoges and not amphetamine derivatives.
In 1983 a group of heroin users attempted a demerol synthesis and obtained instead a compound called MPTP. The product had a similar appearance and melting point, and they injected it expecting a demerol high. In the brain, MPTP decomposes to MPP+ which selectively bonds to and destroys dopamine receptors. These individuals thus prematurely gave themselves Parkinson's disease. MPP+ closely resembles paraquat, a defoliant used by the US government, outside US borders, against marijuana (a bit heavy handed and reckless).
In order to understand the development and behavior of central dopaminergic neurons and molecular mechanisms involved in the degeneration of such neurons in PD and MPTP-induced PD, several investigators have developed an immortalized dopaminergic cell line. The cell line is called MES 23.5 and is derived by fusion of rat embryonic mesencephalon cells with murine N18TG2 neuroblastoma cells. The cell line expresses a complex range of neural properties found in the dopaminergic neurons of the substantia nigra (Crawford et al, 1992), including tyrosine hydroxylase, dopamine synthesis, and conotoxin receptors (control of calcium channels). Only dopamine, and no other catecholamine, is synthesized by the cells. Levels of tyrosine and dopamine are elevated by 3-7 fold with the treatment of dibutyrl-cAMP. This cell line offers several advantages over other cell lines including greater homogeneity (providing more obvious and consistent observations), and susceptibility to both free radical-mediated cytotoxicity and calcium-dependent cell death.
It has been recently proposed that cerebrospinal fluid (CSF) from PD patients may possess substances which are neurotoxic for dopaminergic cells (Klawans et al, 1993; Hao et al, 1995). To define the selectivity, specificity, and property of these cytotoxic factors, investigators have employed MES 23.5 cell cultures to examine cytotoxicity of CSF from PD and non-PD patients. Preliminary studies from 5 of 7 CSF samples from PD patients, but none of 5 CSF samples from control subjects, have shown significant cytotoxic effects on MES 23.5 cells as determined by cell viability assays. The damaged cells demonstrate a pattern of apoptotic morphology including nuclear chromatin condensation and nuclear fragmentation. An approach to identify the cytotoxic factors is underway. These results raise intriguing possibilities for the etiology and pathogenesis of PD.
http://www.namiscc.org/Research/2002/Psychosis.htm
gustatory sweating occurred in 32% of patients
Compensatory sweating is a frequent side effect after thoracoscopic sympathectomy for primary hyperhidrosis. Gustatory sweating is less commonly reported. It is defined as facial sweating when eating certain foods (particularly spicy food or acidic fruits) and has no generally accepted pathophysiologic explanation.
Overall, gustatory sweating occurred in 32% of patients, and the incidence was significantly associated with extent of sympathectomy (p = 0.04). However, because the extent of sympathectomy was always decided by the location of primary hyperhidrosis, the latter may also explain the risk of gustatory sweating. CONCLUSIONS: Gustatory sweating is a frequent side effect after thoracoscopic sympathectomy. This is the first study to report that its incidence is significantly related to the extent of sympathectomy or the location of primary hyperhidrosis. Although there is no pathophysiologic explanation of gustatory sweating, these findings should be considered before planning thoracoscopic sympathectomy and patients should be thoroughly informed.
Ann Thorac Surg. 2006 Mar;81(3):1047.
Overall, gustatory sweating occurred in 32% of patients, and the incidence was significantly associated with extent of sympathectomy (p = 0.04). However, because the extent of sympathectomy was always decided by the location of primary hyperhidrosis, the latter may also explain the risk of gustatory sweating. CONCLUSIONS: Gustatory sweating is a frequent side effect after thoracoscopic sympathectomy. This is the first study to report that its incidence is significantly related to the extent of sympathectomy or the location of primary hyperhidrosis. Although there is no pathophysiologic explanation of gustatory sweating, these findings should be considered before planning thoracoscopic sympathectomy and patients should be thoroughly informed.
Ann Thorac Surg. 2006 Mar;81(3):1047.
Compensatory sweating occurred in 89% of patients and was so severe in 35% that they often had to change their clothes during the day.
Department of Cardiothoracic Surgery, Skejby Sygehus, Aarhus University Hospital, Aarhus, Denmark.
BACKGROUND: Compensatory sweating is a well-known side effect after sympathectomy for hyperhidrosis. It is often claimed to correlate with the extent of sympathectomy, but results from the literature are conflicting, and few have actually considered differences in the intensity of compensatory sweating. METHODS: A total of 158 patients underwent thoracoscopic sympathectomy for primary hyperhidrosis or blushing, or both. Sympathectomy was performed bilaterally at Th2 for facial hyperhidrosis/blushing (n = 49), Th2-3 for palmar hyperhidrosis (n = 62), and Th2-4 for axillary hyperhidrosis (n = 47). RESULTS: Follow-up by questionnaire was possible in 94% of patients after a median of 26 months. Compensatory sweating occurred in 89% of patients and was so severe in 35% that they often had to change their clothes during the day. The frequency of compensatory sweating was not significantly different among the three groups, but severity was significantly higher after Th2-4 sympathectomy for axillary hyperhidrosis (p = 0.04). Gustatory sweating occurred in 38% of patients, and 16% of patients regretted the operation.
Ann Thorac Surg. 2004 Aug;78(2):427-31.
BACKGROUND: Compensatory sweating is a well-known side effect after sympathectomy for hyperhidrosis. It is often claimed to correlate with the extent of sympathectomy, but results from the literature are conflicting, and few have actually considered differences in the intensity of compensatory sweating. METHODS: A total of 158 patients underwent thoracoscopic sympathectomy for primary hyperhidrosis or blushing, or both. Sympathectomy was performed bilaterally at Th2 for facial hyperhidrosis/blushing (n = 49), Th2-3 for palmar hyperhidrosis (n = 62), and Th2-4 for axillary hyperhidrosis (n = 47). RESULTS: Follow-up by questionnaire was possible in 94% of patients after a median of 26 months. Compensatory sweating occurred in 89% of patients and was so severe in 35% that they often had to change their clothes during the day. The frequency of compensatory sweating was not significantly different among the three groups, but severity was significantly higher after Th2-4 sympathectomy for axillary hyperhidrosis (p = 0.04). Gustatory sweating occurred in 38% of patients, and 16% of patients regretted the operation.
Ann Thorac Surg. 2004 Aug;78(2):427-31.
Sympathectomy induces adrenergic excitability of cutaneous C-fiber nociceptors
D. F. Bossut, V. K. Shea and E. R. Perl
Department of Physiology, University of North Carolina at Chapel Hill 27599-7545, USA.
1. The effects of ipsilateral removal of the superior cervical ganglion on the subsequent responsiveness of C-fiber polymodal nociceptors (CPMs) of the ear to close-arterial injections of norepinephrine (NE) were evaluated in adult, anesthetized rabbits. 2. In normal unanesthetized rabbits, the two ears were usually at the same temperature. Immediately after the ganglionectomy, the ipsilateral ear was warmer; however, at the time of electrophysiological recordings (4-23 days) the majority of animals had the ipsilateral ear cooler by > or = 1 degree C, suggestive of denervation supersensitivity. 3. NE (50 ng) did not activate any CPMs (n = 28) from intact animals. 4. Seven of 22 CPMs recorded from sympathectomized ears were activated by NE (50 ng). The responses varied considerably but typically consisted of 2-4 impulses in the 60 s after the NE injection. In some instances, repetitive activity continued for many minutes. Such prolonged discharge differs from the adrenergic responses seen after partial nerve damage. 5. The induction of adrenergic excitability in CPMs by sympathectomy is suggested to be a counterpart to postsympathectomy neuralgia in human beings and a possible part of the mechanism leading to sympathetically related pain states.
Journal of Neurophysiology, Vol 75, Issue 1 514-517,
Department of Physiology, University of North Carolina at Chapel Hill 27599-7545, USA.
1. The effects of ipsilateral removal of the superior cervical ganglion on the subsequent responsiveness of C-fiber polymodal nociceptors (CPMs) of the ear to close-arterial injections of norepinephrine (NE) were evaluated in adult, anesthetized rabbits. 2. In normal unanesthetized rabbits, the two ears were usually at the same temperature. Immediately after the ganglionectomy, the ipsilateral ear was warmer; however, at the time of electrophysiological recordings (4-23 days) the majority of animals had the ipsilateral ear cooler by > or = 1 degree C, suggestive of denervation supersensitivity. 3. NE (50 ng) did not activate any CPMs (n = 28) from intact animals. 4. Seven of 22 CPMs recorded from sympathectomized ears were activated by NE (50 ng). The responses varied considerably but typically consisted of 2-4 impulses in the 60 s after the NE injection. In some instances, repetitive activity continued for many minutes. Such prolonged discharge differs from the adrenergic responses seen after partial nerve damage. 5. The induction of adrenergic excitability in CPMs by sympathectomy is suggested to be a counterpart to postsympathectomy neuralgia in human beings and a possible part of the mechanism leading to sympathetically related pain states.
Journal of Neurophysiology, Vol 75, Issue 1 514-517,
Monday, April 28, 2008
blocking the sympathetic system - treatment for social phobia
The connection between psyche and sympathetic nervous system
Timo Telaranta M.D., Ph.D. and Paivi Pohjavaara M.D., Privatix Clinic, Tampere, Finland
In the central nervous system the arousal requires the brain stem, the thalamus and the cortex, attention is maintained in the right frontal lobe; the formation of memories happens in the medial temporal lobe, certain diencephalic nuclei and the basal forebrain. The amygdala rates the emotions of an experience. The limbic system is the centre of the human drives, their regulation requires an intact frontal cortex. The injury in the frontal lobe impairs the executive functions as motivation and attention. The sympathomedullary system and locus coerulaeus are activated in depression, mania, panic disorder and acute phases of schizophrenia. The autonomic nervous system is one of the most important mediators between the mind and the body. It has two roles in this function: the role in basic metabolic function as in energy storage and release, in the control of exocrine secretion and thus intake, in conservation, loss, and transformation of energy the role in behaviour, where the hypothalamus is involved in alert and defense reactions.
The sympathetic system is defined as an energy consumption system and the parasympathetic system is an energy conserving and balancing force. The sympathomedullary system is activated in various mental disorders. The biopsychosocial model is clearly seen in the social phobia. The "fight or flight " response of the sympathetic system can also be seen in the physical signs of the social phobia when the patient is in the centre of attention. With sympathetic overload the patient starts to fear the triggering situations and avoid them. The need-adaptive approach adjusts treatment plans of socially phobic patients who haven't had any help of medication and psychotherapy. It seems possible to treat their symptoms and cut the vicious circle of social phobia blocking the sympathetic system in the upper thoracic level with a surgical procedure. If a patient with the social phobia hasn't had any help of conventional treatment methods such as medication and psychotherapy, the sympathetic block could be a treatment of choice for them
Timo Telaranta M.D., Ph.D. and Paivi Pohjavaara M.D., Privatix Clinic, Tampere, Finland
In the central nervous system the arousal requires the brain stem, the thalamus and the cortex, attention is maintained in the right frontal lobe; the formation of memories happens in the medial temporal lobe, certain diencephalic nuclei and the basal forebrain. The amygdala rates the emotions of an experience. The limbic system is the centre of the human drives, their regulation requires an intact frontal cortex. The injury in the frontal lobe impairs the executive functions as motivation and attention. The sympathomedullary system and locus coerulaeus are activated in depression, mania, panic disorder and acute phases of schizophrenia. The autonomic nervous system is one of the most important mediators between the mind and the body. It has two roles in this function: the role in basic metabolic function as in energy storage and release, in the control of exocrine secretion and thus intake, in conservation, loss, and transformation of energy the role in behaviour, where the hypothalamus is involved in alert and defense reactions.
The sympathetic system is defined as an energy consumption system and the parasympathetic system is an energy conserving and balancing force. The sympathomedullary system is activated in various mental disorders. The biopsychosocial model is clearly seen in the social phobia. The "fight or flight " response of the sympathetic system can also be seen in the physical signs of the social phobia when the patient is in the centre of attention. With sympathetic overload the patient starts to fear the triggering situations and avoid them. The need-adaptive approach adjusts treatment plans of socially phobic patients who haven't had any help of medication and psychotherapy. It seems possible to treat their symptoms and cut the vicious circle of social phobia blocking the sympathetic system in the upper thoracic level with a surgical procedure. If a patient with the social phobia hasn't had any help of conventional treatment methods such as medication and psychotherapy, the sympathetic block could be a treatment of choice for them
Psychosurgery
In the early 20th century, a medical treatment for mental illness, first developed by Portuguese neurologist Egas Moniz, involved damaging the pathways connecting the frontal lobe to the limbic system. Frontal lobotomy (sometimes called frontal leucotomy) successfully reduced distress but at the cost of often blunting the subject's emotions, volition and personality. The indiscriminate use of this psychosurgical procedure, combined with the severe side effects and dangerous nature of the operation gained it a bad reputation and the frontal lobotomy has largely died out as a psychiatric treatment.
More precise psychosurgical procedures are still occasionally used, although are now very rare occurrences. They may include procedures such as the anterior capsulotomy (bilateral thermal lesions of the anterior limbs of the internal capsule) or the bilateral cingulotomy.
More precise psychosurgical procedures are still occasionally used, although are now very rare occurrences. They may include procedures such as the anterior capsulotomy (bilateral thermal lesions of the anterior limbs of the internal capsule) or the bilateral cingulotomy.
Poor regulation of dopamine pathways has been associated with schizophrenia
A report from the National Institute of Mental Health says a gene variant that reduces dopamine activity in the prefrontal cortex is related to poorer performance and inefficient functioning of that brain region during working memory tasks, and to slightly increased risk for schizophrenia.
Dopamine-sensitive neurons in the cerebral cortex are found primarily in the frontal lobes. The dopamine system is associated with pleasure, long-term memory, planning and drive. Dopamine tends to limit and select sensory information arriving from the thalamus to the fore-brain. Poor regulation of dopamine pathways has been associated with schizophrenia.
The so-called executive functions of the frontal lobes involve the ability to recognize future consequences resulting from current actions, to choose between good and bad actions (or better and best), override and suppress unacceptable social responses, and determine similarities and differences between things or events.
The frontal lobes also play an important part in retaining longer term memories which are not task-based. These are often memories with associated emotions, derived from input from the brain's limbic system, and modified by the higher frontal lobe centers to generally fit socially acceptable norms (see executive functions above). The frontal lobes have rich neuronal input from both the alert centers in the brain-stem, and from the limbic regions.
Dopamine-sensitive neurons in the cerebral cortex are found primarily in the frontal lobes. The dopamine system is associated with pleasure, long-term memory, planning and drive. Dopamine tends to limit and select sensory information arriving from the thalamus to the fore-brain. Poor regulation of dopamine pathways has been associated with schizophrenia.
The so-called executive functions of the frontal lobes involve the ability to recognize future consequences resulting from current actions, to choose between good and bad actions (or better and best), override and suppress unacceptable social responses, and determine similarities and differences between things or events.
The frontal lobes also play an important part in retaining longer term memories which are not task-based. These are often memories with associated emotions, derived from input from the brain's limbic system, and modified by the higher frontal lobe centers to generally fit socially acceptable norms (see executive functions above). The frontal lobes have rich neuronal input from both the alert centers in the brain-stem, and from the limbic regions.
Orthostatic Intolerance
The normal response for a change in body position, results in a stabilization to the upright position in approximately sixty seconds. During this process, the normal change in heart rate would include an increase in heart rate of 10 to 15 beats per minute, and an increase in diastolic pressure of 10 mm Hg, with only a slight change in systolic pressure.
For those who are afflicted with Orthostatic Intolerance, there is an excessive increase in heart rate upon standing, resulting in the cardiovascular system working harder to maintain blood pressure and blood flow to the brain.
Upright posture also brings about a neurohumoral response, involving a change in the levels of vasopressin, renin, angiotensin and aldosterone levels - all of which are involved in the regulation of blood pressure.
Additionally, arterial baroreceptors, particularly those in the carotid sinus area, play an important role in the regulation of blood pressure and the response to positional changes. As the heart pumps blood to the body, the left atrium is passively filled with blood as a result of the force exerted by venous blood pressure. The baroreceptors in the left atrium respond, proportionately, to the pressure exerted by this venous blood pressure. Thus, a drop in venous blood pressure will trigger a compensatory response to increase blood pressure.
Any disruption in any of these processes, or their coordination, can result in an inappropriate response to an upright position, and can lead to a series of symptoms.
The symptoms for these conditions may include the following:
Excessive Fatigue
Exercise Intolerance
Recurrent Syncope or Near Syncope
Dizziness
Nausea
Tachycardia
Palpitations
Visual Disturbances
Tremulusness
Weakness - most noticeable in the legs
Chest Discomfort
Shortness of Breath
Mood Swings
Migraines and Other Headaches
Gastrointestinal Problems
National Dysautonomia Research Foundation
http://ndrf.org/orthostat.htm
For those who are afflicted with Orthostatic Intolerance, there is an excessive increase in heart rate upon standing, resulting in the cardiovascular system working harder to maintain blood pressure and blood flow to the brain.
Upright posture also brings about a neurohumoral response, involving a change in the levels of vasopressin, renin, angiotensin and aldosterone levels - all of which are involved in the regulation of blood pressure.
Additionally, arterial baroreceptors, particularly those in the carotid sinus area, play an important role in the regulation of blood pressure and the response to positional changes. As the heart pumps blood to the body, the left atrium is passively filled with blood as a result of the force exerted by venous blood pressure. The baroreceptors in the left atrium respond, proportionately, to the pressure exerted by this venous blood pressure. Thus, a drop in venous blood pressure will trigger a compensatory response to increase blood pressure.
Any disruption in any of these processes, or their coordination, can result in an inappropriate response to an upright position, and can lead to a series of symptoms.
The symptoms for these conditions may include the following:
Excessive Fatigue
Exercise Intolerance
Recurrent Syncope or Near Syncope
Dizziness
Nausea
Tachycardia
Palpitations
Visual Disturbances
Tremulusness
Weakness - most noticeable in the legs
Chest Discomfort
Shortness of Breath
Mood Swings
Migraines and Other Headaches
Gastrointestinal Problems
National Dysautonomia Research Foundation
http://ndrf.org/orthostat.htm
Sunday, April 27, 2008
dopamine receptors are widely expressed because they are involved in the control of locomotion, cognition, emotion
The D2 and D3 receptors vary in certain tissues and species as a result of alternative splicing, and the human D4 receptor gene exhibits extensive polymorphic variation. In the central nervous system, dopamine receptors are widely expressed because they are involved in the control of locomotion, cognition, emotion, and affect as well as neuroendocrine secretion. In the periphery, dopamine receptors are present more prominently in kidney, vasculature, and pituitary, where they affect mainly sodium homeostasis, vascular tone, and hormone secretion. Numerous genetic linkage analysis studies have failed so far to reveal unequivocal evidence for the involvement of one of these receptors in the etiology of various central nervous system disorders. However, targeted deletion of several of these dopamine receptor genes in mice should provide valuable information about their physiological functions.
PHYSIOLOGICAL REVIEWS Vol. 78 No. 1 January 1998, pp. 189-225
Copyright ©1998 The American Physiological Society
Dopamine Receptors: From Structure to Function
CRISTINA MISSALE, S. RUSSEL NASH, SUSAN W. ROBINSON, MOHAMED JABER, AND MARC G. CARON
Departments of Cell Biology and Medicine, Howard Hughes Medical Institute Laboratories, Duke University Medical Center, Durham, North Carolina
PHYSIOLOGICAL REVIEWS Vol. 78 No. 1 January 1998, pp. 189-225
Copyright ©1998 The American Physiological Society
Dopamine Receptors: From Structure to Function
CRISTINA MISSALE, S. RUSSEL NASH, SUSAN W. ROBINSON, MOHAMED JABER, AND MARC G. CARON
Departments of Cell Biology and Medicine, Howard Hughes Medical Institute Laboratories, Duke University Medical Center, Durham, North Carolina
Changes in dopamine D2 receptors and 6-[18F]fluoro-L-3,4-dihydroxyphenylalanine uptake in the brain of 6-hydroxydopamine-lesioned rats
Ishida Y, Kawai K, Magata Y, Takeda R, Hashiguchi H, Abe H, Mukai T, Saji H.
Department of Psychiatry, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan.
We studied tracer distributions in positron emission tomography of ligands for dopamine D1 receptors ([11C]SCH23390) and D2 receptors ([11C]raclopride) and the dopamine precursor analog 6-[18F]fluoro-L-3,4-dihydroxyphenylalanine ([18F]FDOPA), as a measurement of presynaptic dopaminergic function, in the brain after 6-hydroxydopamine lesioning of the medial forebrain bundle in rats. The unilateral lesions were confirmed behaviorally by methamphetamine-induced rotation 2 weeks after lesioning, and the brains were analyzed by tissue dissection following an intravenous bolus of each tracer 3 weeks after lesioning. [11C]Raclopride, but not [11C]SCH23390, showed a higher accumulation in the striatum on the lesion side compared with that on the non-lesioned (intact) side. On the other hand, a lower accumulation of [18F]FDOPA was found in the striatum and cerebral cortex on the lesion side. Our studies demonstrate upregulation of dopamine D2 receptors in the striatum and a decrease in FDOPA uptake in both the striatum and cerebral cortex ipsilateral to the 6-hydroxydopamine lesions. Therefore, the combination of a D2 antagonist and FDOPA may provide a potentially useful method for assessing the effects of dopamine depletion in Parkinson's disease. Copyright 2004 S. Karger AG, Basel.
Neurodegener Dis. 2004;1(2-3):109-12.
Department of Psychiatry, Miyazaki Medical College, University of Miyazaki, Miyazaki, Japan.
We studied tracer distributions in positron emission tomography of ligands for dopamine D1 receptors ([11C]SCH23390) and D2 receptors ([11C]raclopride) and the dopamine precursor analog 6-[18F]fluoro-L-3,4-dihydroxyphenylalanine ([18F]FDOPA), as a measurement of presynaptic dopaminergic function, in the brain after 6-hydroxydopamine lesioning of the medial forebrain bundle in rats. The unilateral lesions were confirmed behaviorally by methamphetamine-induced rotation 2 weeks after lesioning, and the brains were analyzed by tissue dissection following an intravenous bolus of each tracer 3 weeks after lesioning. [11C]Raclopride, but not [11C]SCH23390, showed a higher accumulation in the striatum on the lesion side compared with that on the non-lesioned (intact) side. On the other hand, a lower accumulation of [18F]FDOPA was found in the striatum and cerebral cortex on the lesion side. Our studies demonstrate upregulation of dopamine D2 receptors in the striatum and a decrease in FDOPA uptake in both the striatum and cerebral cortex ipsilateral to the 6-hydroxydopamine lesions. Therefore, the combination of a D2 antagonist and FDOPA may provide a potentially useful method for assessing the effects of dopamine depletion in Parkinson's disease. Copyright 2004 S. Karger AG, Basel.
Neurodegener Dis. 2004;1(2-3):109-12.
S - increase in activity of the adrenal gland.
Depletion and recovery of catecholamines in several organs of rats treated with reserpine.
[My paper] Rubén Martínez-Olivares, Iván Villanueva, Radu Racotta, Manuel Piñón
Depto. de Fisiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Carpio y Plan de Ayala s/n. Col. Santo Tomás, DF. CP. 11340, México.
Chemical sympathectomy with reserpine depletes catecholamines in every neuronal or nonneuronal cell producing a nonspecific temporal sympathectomy. After reserpine administration, most of the drug is distributed to tissues based on their blood flow and would then either be metabolized or be reversibly bound in lipid depots from where it might be released. Consequently, reserpine concentration and the catecholamine-depleting effect in the various tissues are expected to differ according to the route of administration. This study was designed to compare the effects of intraperitoneal (i.p.) and subcutaneous (s.c.) administration of reserpine on catecholamine depletion and recovery in the liver, portal vein, and adrenal gland on days 1, 4, and 10 after reserpine dosage. Catecholamine determinations were extended to 25 days after the treatment only in s.c. reserpine-treated rats and adding samples of heart and brown adipose tissue to the testing. I.p. and s.c. reserpine administration had the same norepinephrine-depleting effect in the portal vein and liver but full recovery was present in both tissues only in i.p. reserpine-treated rats. In the adrenal gland, both routes of administration produced the same depleting and recovery effect of norepinephrine and epinephrine concentrations. A significant temporary overshoot in epinephrine levels was observed several days after s.c. reserpine treatment. Except for the liver, reserpine injected s.c. depleted norepinephrine concentrations significantly in all other tissues up to the end of the experiment. Our results suggest that chemical sympathectomy caused by reserpine administered s.c. produces a generalized and prolonged decrease in peripheral sympathetic activity that could be compensated by an increase in activity of the adrenal gland.
Auton Neurosci. 2006 May 22; : 16723281 (P,S,E,B)
[My paper] Rubén Martínez-Olivares, Iván Villanueva, Radu Racotta, Manuel Piñón
Depto. de Fisiología, Escuela Nacional de Ciencias Biológicas, Instituto Politécnico Nacional, Carpio y Plan de Ayala s/n. Col. Santo Tomás, DF. CP. 11340, México.
Chemical sympathectomy with reserpine depletes catecholamines in every neuronal or nonneuronal cell producing a nonspecific temporal sympathectomy. After reserpine administration, most of the drug is distributed to tissues based on their blood flow and would then either be metabolized or be reversibly bound in lipid depots from where it might be released. Consequently, reserpine concentration and the catecholamine-depleting effect in the various tissues are expected to differ according to the route of administration. This study was designed to compare the effects of intraperitoneal (i.p.) and subcutaneous (s.c.) administration of reserpine on catecholamine depletion and recovery in the liver, portal vein, and adrenal gland on days 1, 4, and 10 after reserpine dosage. Catecholamine determinations were extended to 25 days after the treatment only in s.c. reserpine-treated rats and adding samples of heart and brown adipose tissue to the testing. I.p. and s.c. reserpine administration had the same norepinephrine-depleting effect in the portal vein and liver but full recovery was present in both tissues only in i.p. reserpine-treated rats. In the adrenal gland, both routes of administration produced the same depleting and recovery effect of norepinephrine and epinephrine concentrations. A significant temporary overshoot in epinephrine levels was observed several days after s.c. reserpine treatment. Except for the liver, reserpine injected s.c. depleted norepinephrine concentrations significantly in all other tissues up to the end of the experiment. Our results suggest that chemical sympathectomy caused by reserpine administered s.c. produces a generalized and prolonged decrease in peripheral sympathetic activity that could be compensated by an increase in activity of the adrenal gland.
Auton Neurosci. 2006 May 22; : 16723281 (P,S,E,B)
partial denervation by lesion of peripheral nerve or by tissue destruction induces a change in peripheral nociceptors, making them excitable
Edward R. Perl*
Department of Cell and Molecular Physiology, CB 7545, University of North Carolina, Chapel Hill, NC 27599
Control of expression of molecular receptors for chemical messengers and modulation of these receptors' activity are now established as ways to alter cellular reaction. This paper extends these mechanisms to the arena of pathological pain by presenting the hypothesis that increased expression of alpha -adrenergic receptors in primary afferent neurons is part of the etiology of pain in classical causalgia. It is argued that partial denervation by lesion of peripheral nerve or by tissue destruction induces a change in peripheral nociceptors, making them excitable by sympathetic activity and adrenergic substances. This excitation is mediated by alpha -adrenergic receptors and has a time course reminiscent of experimental denervation supersensitivity. The change in neuronal phenotype is demonstrable after lesions of mixed nerves or of the sympathetic postganglionic supply. Similar partial denervations also produce a substantial increase in the number of dorsal root ganglion neurons evidencing the presence of alpha -adrenergic receptors. The hypothesis proposes the increased presence of alpha -adrenergic receptors in primary afferent neurons to result from an altered gene expression triggered by cytokines/growth factors produced by disconnection of peripheral nerve fibers from their cell bodies. These additional adrenergic receptors are suggested to make nociceptors and other primary afferent neurons excitable by local or circulating norepinephrine and epinephrine. For central pathways, the adrenergic excitation would be equivalent to that produced by noxious events and would consequently evoke pain. In support, evidence is cited for a form of denervation supersensitivity in causalgia and for increased expression of human alpha -adrenergic receptors after loss of sympathetic activity.
Vol. 96, Issue 14, 7664-7667, July 6, 1999
PNAS
Department of Cell and Molecular Physiology, CB 7545, University of North Carolina, Chapel Hill, NC 27599
Control of expression of molecular receptors for chemical messengers and modulation of these receptors' activity are now established as ways to alter cellular reaction. This paper extends these mechanisms to the arena of pathological pain by presenting the hypothesis that increased expression of alpha -adrenergic receptors in primary afferent neurons is part of the etiology of pain in classical causalgia. It is argued that partial denervation by lesion of peripheral nerve or by tissue destruction induces a change in peripheral nociceptors, making them excitable by sympathetic activity and adrenergic substances. This excitation is mediated by alpha -adrenergic receptors and has a time course reminiscent of experimental denervation supersensitivity. The change in neuronal phenotype is demonstrable after lesions of mixed nerves or of the sympathetic postganglionic supply. Similar partial denervations also produce a substantial increase in the number of dorsal root ganglion neurons evidencing the presence of alpha -adrenergic receptors. The hypothesis proposes the increased presence of alpha -adrenergic receptors in primary afferent neurons to result from an altered gene expression triggered by cytokines/growth factors produced by disconnection of peripheral nerve fibers from their cell bodies. These additional adrenergic receptors are suggested to make nociceptors and other primary afferent neurons excitable by local or circulating norepinephrine and epinephrine. For central pathways, the adrenergic excitation would be equivalent to that produced by noxious events and would consequently evoke pain. In support, evidence is cited for a form of denervation supersensitivity in causalgia and for increased expression of human alpha -adrenergic receptors after loss of sympathetic activity.
Vol. 96, Issue 14, 7664-7667, July 6, 1999
PNAS
Bendroflumethiazide; Nadolol Tablets
What should my health care professional know before I receive Bendroflumethiazide; Nadolol?
They need to know if you have any of these conditions:
*
asthma, bronchitis or bronchospasm
*
autoimmune disease such as lupus
*
chest pain (angina)
*
circulation problems, or blood vessel disease (such as Raynaud's disease)
*
depression
*
diabetes
*
electrolyte imbalance (such as low or high levels of potassium in the blood)
*
emphysema, COPD, or other lung disease
*
gout
*
heart disease (such as heart failure or a history of heart attack)
*
kidney disease
*
liver disease
*
muscle weakness or myasthenia gravis
*
pancreatitis
*
pheochromocytoma
*
post-sympathectomy
*
psoriasis
*
thyroid disease
*
unusually slow heartbeat
What should my health care professional know before I receive Bendroflumethiazide; Nadolol?
They need to know if you have any of these conditions:
*
asthma, bronchitis or bronchospasm
*
autoimmune disease such as lupus
*
chest pain (angina)
*
circulation problems, or blood vessel disease (such as Raynaud's disease)
*
depression
*
diabetes
*
electrolyte imbalance (such as low or high levels of potassium in the blood)
*
emphysema, COPD, or other lung disease
*
gout
*
heart disease (such as heart failure or a history of heart attack)
*
kidney disease
*
liver disease
*
muscle weakness or myasthenia gravis
*
pancreatitis
*
pheochromocytoma
*
post-sympathectomy
*
psoriasis
*
thyroid disease
*
unusually slow heartbeat
Supersensitivity of effector cells (smooth muscle) occurs following long-term use, reminiscent of surgical sympathectomy.
Guanethidine and guanadrel
Adverse effects and toxicity: Postural hypotension and decreased blood flow to heart and brain. It causes delayed ejaculaiton in men, increased GI motility and diarrhea. Supersensitivity of effector cells (smooth muscle) occurs following long-term use, reminiscent of surgical sympathectomy.
Adverse effects and toxicity: Postural hypotension and decreased blood flow to heart and brain. It causes delayed ejaculaiton in men, increased GI motility and diarrhea. Supersensitivity of effector cells (smooth muscle) occurs following long-term use, reminiscent of surgical sympathectomy.
The antihypertensive effects of thiazides may be enhanced in the post-sympathectomy patient.
PRODUCT MONOGRAPH
TENORETIC
Antihypertensive Agent
PRECAUTIONS:
The antihypertensive effects of thiazides may be enhanced in the post-sympathectomy patient.
TENORETIC
Antihypertensive Agent
PRECAUTIONS:
The antihypertensive effects of thiazides may be enhanced in the post-sympathectomy patient.
Posterior Left Thoracic Cardiac Sympathectomy by Surgical Division of the Sympathetic Chain: An Alternative Approach to Treatment of the Long QT Syndr
Although high thoracic left Sympathectomy via art anterior surgical approach is a highly efficacious treatment for refractory ventricular arrhythmias in patients with the long QT syndrome, the degree of sympathetic denervation has been variable, success of the operation is influenced by anatomical differences between patients, and Horner's syndrome may result. We hypothesized that interruption of sympathetic input to the heart could be accomplished using a posterior thoracic approach to this variable and often complex anatomy by division of the sympathetic chain rather than by direct destruction of the stellate and superior thoracic ganglia with the more conventional anterior, supraclavicular approach. In addition, the posterior approach should decrease the risk of Horner's syndrome by avoiding the ocular sympathetic efferent nerves. This posterior approach is described in five patients with the long QT syndrome and recurrent ventricular arrhythmias. After a mean follow-up of 18 ± 12 months, all are alive without Homer's syndrome.
* ANDREW E. EPSTEIN11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama,
* MICHAEL J. ROSNER,**Division of Neurosurgery, Department of Surgery, The University of Alabama at Birmingham, Birmingham, Alabama
* GILBERT R. HAGEMAN,****Department of Physiology and Biophysics, The University of Alabama at Birmingham, Birmingham, Alabama
* JAMES H. BAKER, II11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama,
* VANCE J. PLUMB11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, and
* G. NEAL KAY11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama
*
1Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama *Division of Neurosurgery, Department of Surgery, The University of Alabama at Birmingham, Birmingham, Alabama **Department of Physiology and Biophysics, The University of Alabama at Birmingham, Birmingham, Alabama
* ANDREW E. EPSTEIN11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama,
* MICHAEL J. ROSNER,**Division of Neurosurgery, Department of Surgery, The University of Alabama at Birmingham, Birmingham, Alabama
* GILBERT R. HAGEMAN,****Department of Physiology and Biophysics, The University of Alabama at Birmingham, Birmingham, Alabama
* JAMES H. BAKER, II11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama,
* VANCE J. PLUMB11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama, and
* G. NEAL KAY11Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama
*
1Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Birmingham, Alabama *Division of Neurosurgery, Department of Surgery, The University of Alabama at Birmingham, Birmingham, Alabama **Department of Physiology and Biophysics, The University of Alabama at Birmingham, Birmingham, Alabama
Pindolol - inhibition of ejaculaiton
AccessPharmacy.com
... similar to those of surgical sympathectomy, including inhibition of ejaculation, ..... Daily doses of pindolol start at 10 mg; of acebutolol, at 400 mg; ...
www.accesspharmacy.com/Content.aspx?searchStr=acebutolol&aid=2500340 - 139k - Cached - Similar pages
... similar to those of surgical sympathectomy, including inhibition of ejaculation, ..... Daily doses of pindolol start at 10 mg; of acebutolol, at 400 mg; ...
www.accesspharmacy.com/Content.aspx?searchStr=acebutolol&aid=2500340 - 139k - Cached - Similar pages
Potentiation of the antihypertensive effect occurs with ganglionic or peripheral adrenergic blocking drugs and in the post sympathectomy patient
Name of the medicine: BARBLOC
The active ingredient of Barbloc is pindolol.
The active ingredient of Barbloc is pindolol.
Chemical sympathectomy augments the severity of experimental allergic encephalomyelitis
神经肽Y及Th1/Th2细胞与多发性硬化Multiple sclerosis, neuropeptide Y ...
Multiple sclerosis, neuropeptide Y and Th1/Th2 cell .... Chemical sympathectomy augments the severity of experimental allergic encephalomyelitis 《Journal ... scholar.ilib.cn/Abstract.aspx?A=xdkf200521094 - |
Maintenance of blood pressure is mostly dependent on sympathetic “tone”, and the sympathetic nerve innervates the entire vascular bed
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The Japanese Journal of PharmacologyVol. 88 (2002) ,
No. 1 pp.9-13
The significant fall in left circumflex coronary flow was proportional to the decline in external heart work due to sympathectomy both at rest and und
E. Bassenge1, J. Holtz1, W. v. Restorff1 and K. Oversohl1
| (1) | Physiologisches Institut der Ludwig-Maximilian-Universität München, Germany |
Received: 18 April 1973
The exercise capacity and the increase of coronary and systemic hemodynamics under treadmill exercise were studied in 5 dogs, chemically sympathectomized with 6-hydroxy-dopamine.
Completeness of adrenergic denervation was verified by stimulation of the right stellate ganglion, by intravenous administration of tyramine, and by demonstration of supersensitivity to exogenous norepinephrine.
These dogs demonstrated a retarded adaptation of hemodynamics to a sudden start of exercise. A fall in mean arterial pressure below 45 mmHg within 10 to 15 sec lead to collapse. After a recovery period of 60–90 sec, moderate treadmill exercise could be continued; steady state attainment of hemodynamic parameters was considerably delayed.
A steady state of exercise with an O2-consumption (vO2) of 29.6±2.6 ml/min · kg and a cardiac outupt (CO) of 307±16 ml/min · kg was tolerated for at least 20 min.
An increase of vO2 up to 42.0±1.7 ml/min · kg and of CO up to 357±13 ml/min · kg under exercise was tolerated for 5 min with steady state, maximal heart rate being 160±4 min–1 at this level of exercise.
Mean arterial pressure and total peripheral resistance were significantly reduced at rest and during steady state of exercise as compared to controls prior to sympathectomy identical vO2, whereas CO remained unchanged.
The significant fall in left circumflex coronary flow was proportional to the decline in external heart work due to sympathectomy both at rest and under exercise.
Differential Effects of Chemical Sympathectomy on Expression and Activity of Tyrosine Hydroxylase and Levels of Catecholamines and DOPA
Tyrosine hydroxylase (TH) mRNA and activity and concentrations of 3,4-dihydroxyphenylalanine (DOPA) and catecholamines were examined as markers of sympathetic innervation and catecholamine synthesis in peripheral tissues of sympathectomized and intact rats. Chemical sympathectomy with 6-hydroxydopamine (6-OHDA) markedly decreased norepinephrine and to a generally lesser extent TH activities and dopamine in most peripheral tissues (stomach, lung, testis, duodenum, pancreas, salivary gland, spleen, heart, kidney, thymus). Superior cervical ganglia, adrenals and descending aorta were unaffected and vas deferens showed a large 92% decrease in norepinephrine, but only a small 38% decrease in TH activity after 6-OHDA.
Volume 24, Number 1 / January, 1999
JournalNeurochemical Research
Minoru Kawamura1, 2, Joan P. Schwartz1, Takuo Nomura1, Irwin J. Kopin1, David S. Goldstein1, Thanh-Truc Huynh1, Douglas R. Hooper1, Judith Harvey-White1 and Graeme Eisenhofer1
| (1) | Clinical Neuroscience Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, 20892 |
| (2) | Institute of Bio-Active Science, Nippon Zoki Pharmaceutical Co., Ltd. Hyogo, 673-14, Japan |
JournalNeurochemical Research
the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE)
Sammy Bedoui, Sachiko Miyake, Youwei Lin, Katsuichi Miyamoto, Shinji Oki, Noriyuki Kawamura, Annette Beck-Sickinger, Stephan von Hörsten, Takashi Yamamura
Department of Immunology, National Institute of Neuroscience, NCNP, Ogawahigashi, Kodaira, Tokyo, Japan.
Prior studies have revealed that the sympathetic nervous system regulates the clinical and pathological manifestations of experimental autoimmune encephalomyelitis (EAE), an autoimmune disease model mediated by Th1 T cells. Although the regulatory role of catecholamines has been indicated in the previous works, it remained possible that other sympathetic neurotransmitters like neuropeptide Y (NPY) may also be involved in the regulation of EAE. Here we examined the effect of NPY and NPY receptor subtype-specific compounds on EAE, actively induced with myelin oligodendrocyte glycoprotein 35-55 in C57BL/6 mice. Our results revealed that exogenous NPY as well as NPY Y(1) receptor agonists significantly inhibited the induction of EAE, whereas a Y(5) receptor agonist or a combined treatment of NPY with a Y(1) receptor antagonist did not inhibit signs of EAE. These results indicate that the suppression of EAE by NPY is mediated via Y(1) receptors. Furthermore, treatment with the Y(1) receptor antagonist induced a significantly earlier onset of EAE, indicating a protective role of endogenous NPY in the induction phase of EAE. We also revealed a significant inhibition of myelin oligodendrocyte glycoprotein 35-55-specific Th1 response as well as a Th2 bias of the autoimmune T cells in mice treated with the Y(1) receptor agonist. Ex vivo analysis further demonstrated that autoimmune T cells are directly affected by NPY via Y(1) receptors. Taken together, we conclude that NPY is a potent immunomodulator involved in the regulation of the Th1-mediated autoimmune disease EAE.
J. Immunol. 2003 Oct 1;171 (7):3451-8 14500640 (P,S,E,B) Cited:3
J. Immunol. 2003 Oct 1;171 (7):3451-8 14500640 (P,S,E,B) Cited:3
Autonomic innervation of immune organs and neuroimmune modulation.
Autonomic & Autacoid Pharmacology. 23(1):1-25, February 2003.
Mignini, F.; Streccioni, V.; Amenta, F.
Mignini, F.; Streccioni, V.; Amenta, F.
Abstract:
Summary: 1 Increasing evidence indicates the occurrence of functional interconnections between immune and nervous systems, although data available on the mechanisms of this bi-directional cross-talking are frequently incomplete and not always focussed on their relevance for neuroimmune modulation.
2 Primary (bone marrow and thymus) and secondary (spleen and lymph nodes) lymphoid organs are supplied with an autonomic (mainly sympathetic) efferent innervation and with an afferent sensory innervation. Anatomical studies have revealed origin, pattern of distribution and targets of nerve fibre populations supplying lymphoid organs.
3 Classic (catecholamines and acetylcholine) and peptide transmitters of neural and non-neural origin are released in the lymphoid microenvironment and contribute to neuroimmune modulation. Neuropeptide Y, substance P, calcitonin gene-related peptide, and vasoactive intestinal peptide represent the neuropeptides most involved in neuroimmune modulation.
4 Immune cells and immune organs express specific receptors for (neuro)transmitters. These receptors have been shown to respond in vivo and/or in vitro to the neural substances and their manipulation can alter immune responses. Changes in immune function can also influence the distribution of nerves and the expression of neural receptors in lymphoid organs.
5 Data on different populations of nerve fibres supplying immune organs and their role in providing a link between nervous and immune systems are reviewed. Anatomical connections between nervous and immune systems represent the structural support of the complex network of immune responses. A detailed knowledge of interactions between nervous and immune systems may represent an important basis for the development of strategies for treating pathologies in which altered neuroimmune cross-talking may be involved.
NPY in the regulation of autoimmune Th1 cells
Substantial evidence indicates a dysfunctional communication between the sympathetic nervous system and the immune system in Th1-mediated autoimmune diseases, such as rheumatoid arthritis and multiple sclerosis. In this Opinion, we propose that the sympathetic regulation of immunity is not only mediated by catecholamines but also involves neuropeptide Y (NPY), an additional postganglionic SNS transmitter that is shown to modulate various immunological functions in vitro and in vivo. Based on recent experimental findings, we believe that a more precise understanding of the role of NPY in the regulation of autoimmune Th1 cells will provide novel insights into the neuroimmunological basis of autoimmunity.
Available online 20 August 2004.
Available online 20 August 2004.
Sympathetic Neurotransmitters in Joint Inflammation
Available online 5 January 2005.
This article demonstrates the dual pro- and anti-inflammatory role of the sympathetic nervous system (SNS) in inflammatory joint disease (IJD) by way of distinct adrenoceptors. The dual role of the SNS depends on involved compartments, timing of distinct effector mechanisms during the inflammatory process, availability of respective adrenoceptors on target cells, and an intricate shift from β-to-
Saturday, April 26, 2008
Does bilateral thoracic sympathectomy predispose to reflex bronchospasm following tracheal intubation?
A 31 year old old non-smoking woman, 60 kg, withouth a history of allergy or asthma was scheduled for left knee arthroscopy. Two months previously she had an uneventful general anesthetic for bilateral thorascopic sympathectomy to treat essential hyperhidrosis.
Immediately following intubation, ventilation became difficult. Chest auscultation revealed bilateral expiratory wheezing associated with decreased air entry and increased airway pressure up to 60 cm H2O. Oxygen saturation, as monitored by pulse oximetry, decreased from 100% to 80%.
The severe bronchospams occured immediately following tracheal intubation, suggesting that it may have been a reflex response which was triggered by instrumentation of the airway under light level of anesthesia.
Sympathectomy results in a decrease of plasma norepinephrine, and parasympathetic predominance which may increase airway resistance.
Thus, patients with essential hyperhidrosis who have undergone bilateral thoracic sympathectomy, may be more liable to develop reflex bronchospams under light levels of anesthesia.
Ahed Zeidan MD
Nazih Nahle MD
Anis Baraka MD FRCA
Sahel General Hospital, American Universisty of Beirut Medical Center
Immediately following intubation, ventilation became difficult. Chest auscultation revealed bilateral expiratory wheezing associated with decreased air entry and increased airway pressure up to 60 cm H2O. Oxygen saturation, as monitored by pulse oximetry, decreased from 100% to 80%.
The severe bronchospams occured immediately following tracheal intubation, suggesting that it may have been a reflex response which was triggered by instrumentation of the airway under light level of anesthesia.
Sympathectomy results in a decrease of plasma norepinephrine, and parasympathetic predominance which may increase airway resistance.
Thus, patients with essential hyperhidrosis who have undergone bilateral thoracic sympathectomy, may be more liable to develop reflex bronchospams under light levels of anesthesia.
Ahed Zeidan MD
Nazih Nahle MD
Anis Baraka MD FRCA
Sahel General Hospital, American Universisty of Beirut Medical Center
Hypoxaemia is of a major concern during thorascopic sympathectomy
Hypoxaemia is of a major concern during thorascopic sympathectomy. However, the pathophysiology of hypoxaemia and consequent decrease in SpO2 differs between the two anaesthetic techniques.
The normal physiological response to massive atelectasis is an increase in pulmonary vascular resistance (hypoxic pulmonary vasoconstriction) with re-routing of blood to well ventilated lung zones and consequent improvement in PaO2. HOWEVER, DURING ENDOBRONCHIAL ANAESTHESIA FOR THORACIC SYMPATHECTOMY THERE IS AN APPARENT FAILURE OF THIS COMPENSATORY MECHANISM. When more then 70% of the lung is atelectatic, compensation by hypoxic pulmonary vasoconstriction appears ineffective.
During carbon dioxide insufflation using endobronchial intubation, Hartrey and colleagues reported a decrease in systolic arterial pressure of >20mm Hg in 21% of patients. Similarly we have reported sudden hypotension and bradycardia after injudicious carbon dioxide insufflation.
Although extremely rare, sudden cardiac arrest has been reported after left T2-3 sympathetic nerve transection. While the exact pathophysiology of this occurence is unclear, it is postulated that before complete transection of the sympathetic trunk, continuous sympathetic stimulation to the stellate ganglions results in a reduction in the ventricular finrillation threshold, arrhythmia and cosequent cardiac arrest.
In an iteresting study of the delayed cardiac effects of T2-$ symtpathectomy, Drott and colleagues demonstrated significantly reduced heart rate at rest, and during both exercise and the recovery phase of exercise. Changes is the electrical axis and shortening of the QT interval have also been reported.
Irrespective of the technique used the reported incidence of postoperative pneumpthorax is variable, occuring in 2-15% of cases.
In a study by Gothberg, Drott and Claes, postoperative chest x-ray after 1274 procedures, in 602 patients demonstrated that a small apical pneumothroax was a usual occurence.
Conclusion: Because of the anaesthetic implications and possible surgical complications, many surgeons are reluctant to perform transthoracic sympathectomy.
British Journal of Anaesthesia 1997; 79: 113-119
B. Fredman, D. Olsfanger and R. Jedeikin
Left, but not right, one-lung ventilation causes hypoxemia during endoscopic transthoracic sympathectomy
Anesth Analg 2000;90:28
© 2000 International Anesthesia Research Society
Seiji Watanabe, MD , Eiko Noguchi, MD , Shinichi Yamada, MD , Nobuya Hamada, MD , and Tatsuhiko Kano, MD
© 2000 International Anesthesia Research Society
CARDIOVASCULAR ANESTHESIA
Sequential Changes of Arterial Oxygen Tension in the Supine Position During One-Lung Ventilation
Department of Anesthesiology, Kurume University School of Medicine, Fukuoka, Japan
Implications: Close observation and prompt counteractions including termination of one-lung ventilation (OLV) are crucial for patients under OLV in the supine position, because life-threatening hypoxemia frequently occurs approximately 10 min after starting OLV, even under 100% oxygen inhalation. The left semilateral decubitus position was as effective as the left lateral decubitus position in avoiding life-threatening hypoxemia during OLV.
Incidence of chest wall paresthesia after needlescopic video-assisted thoracic surgery for palmar hyperhidrosis
Department of Surgery, Division of Cardiothoracic Surgery, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, Hong Kong SAR, China
Received 5 September 2004; received in revised form 28 September 2004; accepted 22 October 2004.
* Corresponding author. Tel.: +86 852 2632 2629; fax: +86 852 2647 8273. (E-mail: yimap@cuhk.edu.hk).
The effects of hypoxemia, G-6-PD deficiency and sympathectomy might all add to the development of acute pulmonary edema
Transaxillary endoscopic sympathectomy of thoracic ganglia (T2-T3) has recently gained wider acceptance as the treatment of choice for palmar hyperhidrosis. It requires one-lung ventilation to facilitate the surgery. One-lung ventilation, however, is not without complications, among which acute pulmonary edema has been reported. In this case report, we present a patient with palmar hyperhidrosis complicated by glucose-6-phosphate dehydrogenase (G-6-PD) deficiency, who received bilateral endoscopic sympathectomy under alternate one-lung anesthesia, and developed acute pulmonary edema immediately after recruitment of the successive collapsed lung. The effects of hypoxemia, G-6-PD deficiency and sympathectomy might all add to the development of acute pulmonary edema secondary to reexpansion of each individual lung after alternate one-lung ventilation. The possibilities of the inferred causes are herein discussed.
Source: Acta Anaesthesiologica Scandinavica, Volume 45, Number 1, January 2001
Haemodynamic changes during thoracoscopic surgery
Haemodynamic changes during thoracoscopic surgery: The effects of one-lung ventilation compared with carbon dioxide insufflation.
Brock, H. 1; Rieger, R. 2; Gabriel, C. 3; Polz, W. 4; Moosbauer, W. 1; Necek, S. 5
Main Articles
Anaesthesia. 55(1):10-16, January 2000.Brock, H. 1; Rieger, R. 2; Gabriel, C. 3; Polz, W. 4; Moosbauer, W. 1; Necek, S. 5
Abstract:
Summary: We investigated the haemodynamic and respiratory effects of one-lung ventilation and carbon dioxide insufflation in 13 adult patients undergoing video-assisted thoracoscopy. Cardiorespiratory variables were determined during carbon dioxide insufflation at intrahemithoracic pressures of 5, 10 and 15 mmHg, and after 5 and 15 min of one-lung ventilation. Carbon dioxide insufflation was associated with a clear deterioration in circulatory function. The cardiac index decreased subsequent to increasing intrathoracic pressures. The mean cardiac index (SD) at pressures of 10 and 15 mmHg was 1.86 (0.39) and 1.52 (0.46), respectively, and may be compared with the reduced venous return consistent with tension pneumothorax. One-lung ventilation did not affect haemodynamic variables but reduced arterial oxygenation indices (PaO2/FIO2) from 424.29 (160.79) after induction of anaesthesia, to 207.72 (125.50) after 5 min and 172.04 (72.03) after 15 min of one-lung ventilation, respectively. The oxygenation index was not influenced by intrahemithoracic carbon dioxide insufflation. One-lung ventilation via a double-lumen endobronchial tube is safe and convenient for video-assisted thoracoscopic surgery. It has no further consequences on haemodynamic variables, whereas the compression of the lung by carbon dioxide insufflation may cause circulatory dysfunction.
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