Friday, April 18, 2008
Calcitonin gene-related peptide and substance P contribute to reduced blood pressure
1Department of Medicine, Texas A&M University System Health Science Center College of Medicine and Scott & White Health System, Temple, Texas; 2Department of Surgery, University of Texas Medical Branch, Galveston, Texas; and 3Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan
Submitted 21 September 2004 ; accepted in final form 4 May 2005
CGRP and substance P (SP) are produced in dorsal root ganglia (DRG) sensory neurons and modulate vascular tone. Sympathetic and sensory nerves compete for NGF, a potent stimulator of CGRP and SP, and it has been suggested that sympathetic hyperinnervation in spontaneously hypertensive rats may reduce the availability of NGF to sensory nerves, thus reducing CGRP and SP. The purpose of this study was to determine whether destruction of peripheral sympathetic nerves in normal rats would increase the availability of NGF for sensory neurons and enhance expression of CGRP and SP. Sympathectomy was produced in rats by guanethidine sulfate administration. Control rats received saline. Sympathectomized rats displayed reductions in blood pressure (BP) and atria norepinephrine levels, whereas NGF levels in the DRG, spleen, and ventricles were increased. Sympathectomy also enhanced CGRP and SP mRNA and peptide content in DRG. Administration of CGRP and SP receptor antagonists increased the BP in sympathectomized rats but not in the controls. Thus sympathectomy enhances sensory neuron CGRP and SP expression that contributes to the BP reduction.
Substance P
Guanethidine sympathectomy increases substance P concentration in the superior sympathetic ganglion of adult rats
Auteur(s) / Author(s)
BENARROCH E. E. ; ZOLLMAN P. J. ; SCHMELZER J. D. ; NELSON D. K. ; LOW P. A. ;Affiliation(s) du ou des auteurs / Author(s) Affiliation(s)
Mayo clin., dep. neurology, Rochester MN 55905, ETATS-UNISRésumé / Abstract
Adult rats received intraperitoneal injections of guanethidine or saline for 5 weeks. Six to 8 weeks following completion of treatment, concentrations of substance P and neuropeptide Y (NPY) were measured by radioimmunoassay in the superior cervical ganglion (SCG) and thoracic spinal cord. The SCG was also immunostained for NPY and substance P. No differences were observed in thoracic spinal cord content of either NPY or substance P. We observed depletion of NPY immunoreactive neurons and NPY levels in the SCG, and pharmacologic evidence of postganglionic denervation in guanethidine-treated rats
sympathectomy also results in upregulation of CGRP in the trigeminovascular system
In addition, sympathectomy also results in upregulation of CGRP in the trigeminovascular system.
The Headaches - Google Books Result
by Jes Olesen - 2006 - Medical - 1200 pages
Following surgical sympathectomy, a marked increase of CGRP-containing fibres was seen in all tissues studied
Following surgical sympathectomy, a marked increase of CGRP-containing fibres was seen in all tissues studied.
The morphological relationship between sensory and sympathetic nerves was studied in tissues of the eye and the oral cavity following chronic sympathetic or sensory denervation. Immunoreactivities for calcitonin gene-related peptide (CGRP) and tyrosine hydroxylase (TH) were used as indexes to assess the changes of the two nerve populations after denervation.
Morphological changes of sensory CGRP-immunoreactive and sympathetic nerves in peripheral tissues following chronic denervation
| Journal | Histochemistry and Cell Biology |
| Publisher | Springer Berlin / Heidelberg |
| ISSN | 0948-6143 (Print) 1432-119X (Online) |
| Issue | Volume 86, Number 1 / January, 1986 |
Following surgical sympathectomy, a marked increase of CGRP-containing fibres was seen in all tissues studied, while TH-imunoreactive fibres were totally depleated. Conversely, after capsaicin treatment, an increase of TH-immunoreactive nerves was found in the same tissues, concomitant with a sharp decrease of CGRP-immunoreactive nerves. These changes were particularly evident in iridial stroma and around blood vessels in all tissue, where sensory and sympathetic nerves have a closely overlapping distribution pattern.
The altered proportion of sensory peptide-and catecholamine-containing nerves following sympathetic and sensory denervation suggest that there is a reciprocal trophic influence between the two nerve subsets, possibly with the intervention of neurotrophic substances such as nerve growth factor. These results indicate a close interaction between sensory peptidergic and sympathetic nervous systems in peripheral organs.
Sympathectomy-induced increases in calcitonin gene-related peptide (CGRP)-, substance P- and vasoactive intestinal peptide
Sympathectomy-induced increases in calcitonin gene-related peptide (CGRP)-, substance P- and vasoactive intestinal peptide (VIP)-levels in parotid and submandibular glands of the rat.
Ekström J, Ekman RArch Oral Biol. 2005 Oct;50(10):909-17. Epub 2005 Mar 23.
The neuropeptide contents of rat salivary glands were increased four weeks after sympathetic postganglionic denervation (but not after preganglionic denervation): calcitonin gene-related peptide (CGRP) by 400 and 65% in the parotid and submandibular glands, respectively; substance P by 30% in the submandibular gland; and vasoactive intestinal peptide (VIP) by 30% in the parotid gland. The sensory neurotoxin capsaicin prevented the expected increases of CGRP and substance P in the submandibular glands and of VIP in the parotid glands. The CGRP-increase in the parotid gland was, however, only reduced (by 65%). Parasympathetic otic ganglionectomy reduced the peptide levels in the parotid glands (CGRP--50%, VIP--98% and substance P--99%). From these residual levels, CGRP increased almost 8-fold and substance P 3-fold in response to the sympathetic denervation, while VIP was unaffected. In the parasympathetically denervated glands, the capsaicin-sensitive contribution to the CGRP-response to sympathetic denervation was roughly estimated to be more than 25% but less than 40%, while the corresponding contribution to the substance P-response was roughly estimated to be more than 6% but less than 58%. Most likely not only CGRP/substance P-containing sensory C-fibres (submandibular and parotid glands) but also parasympathetic VIP-containing secretomotor and vasomotor fibres (parotid glands) contributed to the capsaicin-sensitive response to sympathetic denervation.
Upregulation of proinflammatory cytokines and nerve growth factor ...
Upregulation of proinflammatory cytokines and nerve growth factor by intraplantar injection of capsaicin in rats
N. E. Saadé *†, C. A. Massaad *, C. I. Ochoa-Chaar †, S. J. Jabbur †, B. Safieh-Garabedian ‡ and S. F. Atweh §
Departments of * Human Morphology, † Physiology and § Internal Medicine, Faculty of Medicine and ‡ Department of Biology, Faculty of Arts and Sciences, American University of Beirut, Beirut, Lebanonhttp://jp.physoc.org/cgi/content/abstract/545/1/241
Thursday, April 17, 2008
Following sympathectomy the basal t-PA activity in plasma was 70% less than controls
Additional evidence that the sympathetic nervous system regulates the vessel wall release of tissue plasminogen activator.
Wang, Y.; Jiang, X.; Hand, A. R.; Gilles, C.; Kirk, J.; Cone, R. E.; O'Rourke, J.
It is established that sympathetic neurons can synthesize, transport and store tissue plasminogen activator (t-PA) within axon terminals in the smooth muscle of vessel walls. Moreover, sympathetic excitations (e.g. physical and mental stress) are known to induce an acute release of t-PA into the circulation. However, relatively little is known about the nature and extent of sympathetic nervous system involvement in the release process per se. We inquired whether a chemical sympathectomy will alter the release of t-PA into the blood, and the intrinsic release of stored t-PA from isolated whole vessel explants. A long-term sympathectomy was induced in adult Sprague-Dawley rats by injection of guanethidine during a 5-week course. The destruction of ganglion neurons and vessel wall axons was verified immunohistochemically. t-PA release was assayed as the free activity in hind limb plasma and explant culture medium. Following sympathectomy: (i) the basal t-PA activity in plasma was 70% less than controls (2.92 +/- 1.96 versus 9.33 +/- 1.72 IU/ml;P <= 0.001); (ii) the acute release from isolated vessels induced by bradykinin or phenylephrine was comparably reduced; and (iii) the greatest reductions occurred in densely innervated small vessel explants. The results provide new support for an autonomic regulation of neural t-PA release into the vessel wall matrix and blood of densely innervated thin-walled microvessels.
Original Articles
Blood Coagulation & Fibrinolysis. 13(6):471-481, September 2002.Wang, Y.; Jiang, X.; Hand, A. R.; Gilles, C.; Kirk, J.; Cone, R. E.; O'Rourke, J.
It is established that sympathetic neurons can synthesize, transport and store tissue plasminogen activator (t-PA) within axon terminals in the smooth muscle of vessel walls. Moreover, sympathetic excitations (e.g. physical and mental stress) are known to induce an acute release of t-PA into the circulation. However, relatively little is known about the nature and extent of sympathetic nervous system involvement in the release process per se. We inquired whether a chemical sympathectomy will alter the release of t-PA into the blood, and the intrinsic release of stored t-PA from isolated whole vessel explants. A long-term sympathectomy was induced in adult Sprague-Dawley rats by injection of guanethidine during a 5-week course. The destruction of ganglion neurons and vessel wall axons was verified immunohistochemically. t-PA release was assayed as the free activity in hind limb plasma and explant culture medium. Following sympathectomy: (i) the basal t-PA activity in plasma was 70% less than controls (2.92 +/- 1.96 versus 9.33 +/- 1.72 IU/ml;P <= 0.001); (ii) the acute release from isolated vessels induced by bradykinin or phenylephrine was comparably reduced; and (iii) the greatest reductions occurred in densely innervated small vessel explants. The results provide new support for an autonomic regulation of neural t-PA release into the vessel wall matrix and blood of densely innervated thin-walled microvessels.
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Altered dopamine beta-hydroxylase (DBH) activity has been reported in mood disorders. Plasma DBH is reduced in major depression with psychosis
Plasma dopamine beta-hydroxylase activity in psychotic and non-psychotic post-traumatic stress disorder
Authors: Hamner M.B.1; Gold P.B.
Source: Psychiatry Research, Volume 77, Number 3, 27 February 1998 , pp. 175-181(7)
Recognition and treatment of comorbid chronic psychotic symptoms in post-traumatic stress disorder (PTSD) has become of increasing clinical interest. Altered dopamine beta-hydroxylase (DBH) activity has been reported in mood disorders. Plasma DBH is reduced in major depression with psychosis and elevated in bipolar disorder with psychosis compared with their respective non-psychotic diagnostic groups. DBH is likely a trait marker with interindividual variations secondary to genetic polymorphism. We therefore evaluated DBH activity in PTSD patients with and without psychotic features and compared these groups with age- and gender-matched control subjects. Vietnam combat veterans with PTSD (n=19) (including patients with and without psychotic features) and normal control subjects (n=22) had plasma DBH enzyme activity assayed photometrically. DBH was significantly higher in patients with PTSD with psychotic features than in patients without psychotic features (80.6±13.4 vs. 42.1±7.3 mM/min, P<0.01)>P<0.01).>
Rheumatoid arthritis and Autonomic Neuropathy
Rheumatoid arthritis, systemic lupus erythematosus, and connective tissue disorders
Rheumatoid arthritis, systemic lupus erythematosus, and other connective tissue disorders may have abnormalities of sympathetic postganglionic function. Some of these patients may have autoantibodies to ganglionic acetylcholine receptors. Autoimmune thyroiditis, as with chronic thyroiditis and Hashimoto thyroiditis, can be associated with some features of Sjögren syndrome such as xerostomia. Patients with systemic sclerosis and mixed connective tissue disorder may have abnormalities of autonomic functioning of esophageal motor activity.
Autonomic Neuropathy
Chronic idiopathic anhidrosis (Mia: one of the side-effects of sympathectomy)
Chronic idiopathic anhidrosis is an acquired generalized loss of sweating without other autonomic features.
Autonomic diseases: clinical features and laboratory evaluation
Minimally invasive endoscopic techniques for sympathectomy often are .... of the enzyme dopamine beta-hydroxylase (DBH), which converts dopamine into ...
jnnp.bmjjournals.com/cgi/content/full/74/suppl_3/iii31 -Similar pages - Note this
jnnp.bmjjournals.com/cgi/content/full/74/suppl_3/iii31 -
Autonomic dysfunction and multiple sclerosis
Multiple Sclerosis, Vol. 7, No. 5, 327-334 (2001)
DOI: 10.1177/135245850100700509
© 2001 SAGE Publications
Peter Flachenecker
Karlheinz Reiners
Miriam Krauser
Annalaska Wolf
Klaus V Toyka
Background: Autonomic dysfunction is frequently observed in patients with multiple sclerosis (MS) but the evolution over time and the relationship to clinical characteristics are not yet established.
Objectives: We investigated the correlation of disease activity and progression of disability with composite scores of cardiovascular autonomic dysfunction and serum levels of catecholamines in a cross-sectional study of patients with clinically active and clinically stable MS.
Results: In the cross-sectional study, the number of patients with at least one abnormal sympathetic test was higher in the `active' patient group (39%) than in healthy controls (8%, P50.02) or `stable' patients (0%, P50.04), while no difference was seen in the parasympathetic score. Median catecholamine levels were significantly lower in `active' MS patients than in those with stable disease (norepinephrine, 204 ng/l (interquartile range 158-310 ng/l) vs 363 ng/l (269-507 ng/l), P50.02 and epinephrine, 23 ng/l (16-28 ng/l) vs 32 ng/l (24-107 ng/l), P50.04). In the subgroup of patients studied longitudinally, parasympathetic but not sympathetic dysfunction increased slightly during the follow-up period, with a significant correlation to the increase in clinical disability (r=0.7, P50.002).
Conclusions: Parasympathetic dysfunction was closely related to the progression of disability in patients with MS. In contrast, sympathetic dysfunction was associated to the clinical activity of MS. This is in line with previous observations suggesting that the autonomic nervous system may be intimately linked with the disordered immune regulation in MS.
DOI: 10.1177/135245850100700509
© 2001 SAGE Publications
Autonomic dysfunction in multiple sclerosis is related to disease activity and progression of disability
Karlheinz Reiners
Miriam Krauser
Annalaska Wolf
Klaus V Toyka
Background: Autonomic dysfunction is frequently observed in patients with multiple sclerosis (MS) but the evolution over time and the relationship to clinical characteristics are not yet established.
Objectives: We investigated the correlation of disease activity and progression of disability with composite scores of cardiovascular autonomic dysfunction and serum levels of catecholamines in a cross-sectional study of patients with clinically active and clinically stable MS.
Results: In the cross-sectional study, the number of patients with at least one abnormal sympathetic test was higher in the `active' patient group (39%) than in healthy controls (8%, P50.02) or `stable' patients (0%, P50.04), while no difference was seen in the parasympathetic score. Median catecholamine levels were significantly lower in `active' MS patients than in those with stable disease (norepinephrine, 204 ng/l (interquartile range 158-310 ng/l) vs 363 ng/l (269-507 ng/l), P50.02 and epinephrine, 23 ng/l (16-28 ng/l) vs 32 ng/l (24-107 ng/l), P50.04). In the subgroup of patients studied longitudinally, parasympathetic but not sympathetic dysfunction increased slightly during the follow-up period, with a significant correlation to the increase in clinical disability (r=0.7, P50.002).
Conclusions: Parasympathetic dysfunction was closely related to the progression of disability in patients with MS. In contrast, sympathetic dysfunction was associated to the clinical activity of MS. This is in line with previous observations suggesting that the autonomic nervous system may be intimately linked with the disordered immune regulation in MS.
Dopamine beta-hydroxylase deficiency impairs cellular immunity
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DBH deficiency - depresssion and schizophrenia
Since norepinephrine and its receptor sites have long been postulated to play a role in a number of psychiatric disorders, the essentially normal mood and mental status of adult DBH-deficiency subjects so far encountered has elicited great interest among investigators in the area of depression and schizophrenia. http://www.mc.vanderbilt.edu/root/vumc.php?site=adc&doc=4792
Vanderbilt Autonomic Dysfunction Center
Norepinephrine and epinephrine are crucial determinants of minute-to-minute neural regulation of blood pressure and are also present at crucial central nervous system sites likely to be involved in a variety of behaviors. Norepinephrine and epinephrine thus seem so important to human beings that it seemed unlikely for many years that subjects without these catecholamines would survive the perinatal period and develop to adulthood.
This view has changed with recognition of a congenital syndrome of severe orthostatic hypotension, noradrenergic failure, and ptosis of the eyelids in two young adults. The syndrome differs from familial dysautonomia and various other autonomic disorders seen in adults in that the defect can be localized to the noradrenergic and adrenergic tissues. There is virtual absence of norepinephrine, epinephrine, and their metabolites. However, there is greatly increased dopamine in plasma, cerebrospinal fluid, and urine.
As children, DBH deficient patients have had a markedly reduced ability to exercise, perhaps because of hypotension engendered by the physical exertion. Because of occasional syncope, anticonvulsive medications have been given in some patients, even though no abnormality was seen on the electroencephalogram. Symptoms have generally worsened in late adolescence and by early adulthood, patients complain of profound orthostatic hypotension, especially early in the day and during hot weather or after alcohol ingestion. In addition to ptosis of the eyelids, there is reduced exercise tolerance, a tendency for nasal stuffiness to occur, especially in the supine posture. A male patient had appropriate erectal function, but retrograde rather than antegrade ejaculation. Presyncopal symptoms in these patients have included dizziness, blurred vision, dyspnea, nuchal discomfort, and occasionally chest pain.
Dopamine beta-hydroxylase deficiency
Dopamine beta-hydroxylase deficiency is a very rare
form of primary autonomic failure characterized by a
complete absence of noradrenaline and adrenaline in plasma
together with increased dopamine plasma levels resulting from
heterogenous molecular alterations of DbH gene.
DbH deficiency is characterized by by cardiovascular disorders
and severe orthostatic hypotension.
Children with DbH deficiency often exhibit reduced ability to exercise
because of blood pressure inadaptation with exertion and syncope.
Symptoms usually worsen during adulthood with severe orthostatic
hypotension, eyelid ptosis, nasal stuffiness and sexual disorders.
Authors: Prof. Jean-Michel Senard, Dr Philippe Rouet
INSERM Unit 586, Insittut Louis Bugnard, C.H.U. Rangueil, 31054,
Toulouse Cedex, France
July 2005
form of primary autonomic failure characterized by a
complete absence of noradrenaline and adrenaline in plasma
together with increased dopamine plasma levels resulting from
heterogenous molecular alterations of DbH gene.
DbH deficiency is characterized by by cardiovascular disorders
and severe orthostatic hypotension.
Children with DbH deficiency often exhibit reduced ability to exercise
because of blood pressure inadaptation with exertion and syncope.
Symptoms usually worsen during adulthood with severe orthostatic
hypotension, eyelid ptosis, nasal stuffiness and sexual disorders.
Authors: Prof. Jean-Michel Senard, Dr Philippe Rouet
INSERM Unit 586, Insittut Louis Bugnard, C.H.U. Rangueil, 31054,
Toulouse Cedex, France
July 2005
Serum dopamine-beta-hydroxylase and depression
Friedhelm Lamprecht1, Michael H. Ebert1, Ibrahim Turek1, 2 and Irwin J. Kopin1
| (1) | Laboratory of Clinical Science, NIMH, 20014 Bethesda, Maryland |
| (2) | Maryland Psychiatric Research Center, Catonsville, Maryland |
Received: 18 June 1974
Abstract Serum dopamine-beta-hydroxylase (DBH) activity was studied in unipolar and bipolar depressed patients who were free of medication and in normal controls. No significant difference was found. A second group of depressed patients were studied during a course of electroconvulsive shock treatment (ECT). A small, but significant, increase in DBH activity was found 5 min after a single modified convulsion, suggesting release of DBH into the circulation. Also a small, but significant, increase in the baseline level of DBH activity was found at the ninth treatment compared to the first treatment. A single electroconvulsive shock administered to rats produced a significant elevation of both plasma epinephrine and norepinephrine at 1 and 5 min post convulsion and a significant, but smaller, elevation of plasma DBH at 5 min post convulsion in adrenalectomized rats.
Key words Electroconvulsive Shock Treatment - Serum Dopamine-Beta-Hydroxylase - Depression - Catecholamines - Sympathetic Nervous System
Serum dopamine-beta-hydroxylase in depressed patients and the effect of electroconvulsive shock treatment
| Journal | Psychopharmacology |
| Publisher | Springer Berlin / Heidelberg |
| ISSN | 0033-3158 (Print) 1432-2072 (Online) |
| Issue | Volume 40, Number 3 / September, 1974 |
Sympathectomy resulted in marked reduction of dopamine beta-hydroxylase immunoreactivity
dopamine beta-hydroxylase
(Dbh-/-), the enzyme responsible for synthesizing norepinephrine and epinephrine from dopamine,
Dbh - dopamine beta hydroxylase
Sympathectomy resulted in marked reduction of dopamine beta-hydroxylase immunoreactivity with no appreciable change in galanin immunoreactivity. ...www.ihop-net.org/UniPub/iHOP/gs/321789.html - 342k
Serum Dopamine-Beta-Hydroxylase Activity -- WEINSHILBOUM and ...
Serum Dopamine-beta-Hydroxylase: Decrease after Chemical Sympathectomy Science, September 3, 1971; 173(4000): 931 - 934. [Abstract] [PDF] ...circres.ahajournals.org/
NASA Technical Reports Server
Anti-dopamine beta-hydroxylase immunotoxin administration produces a rapid, irreversible sympathectomy. NASA Center: NASA (non Center Specific) ...ntrs.nasa.gov/
Serum Dopamine-beta-Hydroxylase (DBH) Activity and Blood Pressure ...
Serum Dopamine-beta-Hydroxylase (DBH) Activity ..... Weinshilboum R, Axelrod J: Serum dopamine-^-hydroxylase: Decrease after chemical sympathectomy. ...www.psychosomaticmedicine.org/cgi/reprint/36/4/298.pdf
dopamine-ß -hydroxylase activity in the sympathetic ganglia is blocked by surgical decentralization
Copyright © 1970 by the National Academy of Sciences
Neurally Mediated Increase in Dopamine-ß -hydroxylase Activity
The development of a sensitive and specific enzymatic assay for dopamine-ß -hydroxylase has enabled us to measure the activity of this enzyme in several tissues where it has not previously been measured. The administration of reserpine leads to an increase in dopamine-ß -hydroxylase activity in the rat adrenal, heart, salivary gland, and in sympathetic ganglia. The increase in the heart is preceded by a small but significant fall. We have confirmed the increase in tyrosine hydroxylase which follows the administration of reserpine and have found that the activity of phenylethanolamine-N-methyltransferase also increases after administration of this drug. The activities of two enzymes not involved in the synthesis of catecholamines, monoamine oxidase and lactate dehydrogenase, are not affected by reserpine treatment. The rise of dopamine-ß -hydroxylase activity in the sympathetic ganglia is blocked by surgical decentralization.
chemical sympathectomy with 6-hydroxy-dopamine reproduces many of the ocular phenomena of surgical sympathectomy
Anterior Segment Chemical Sympathectomy by 6-Hydroxy-Dopamine
I. Effect on Intraocular Pressure and Facility of Outflow
1 Department of Ophthalmology, Tulane University School of Medicine, New Orleans, La.
Histofluorometric techniques have confirmed that topical ocular application of 6-hydroxydopamine, a norepinephrine congener, causes a selective and reversible destruction of sympathetic nerve terminals in the anterior segment. An investigation of the effects of "chemical sympathectomy" on the pupil, intraocular pressure, and facility of outflow showed: the pupil underwent a sequence of changes characteristic of surgical sympathetic denervation, but with a different time course; the intraocular pressure .was significantly lowered, transiently in rabbits and of longer duration in monkeys; the facility of outflow was transiently increased in monkeys and probably in rabbits; the episcleral venous pressure was unchanged in both species. It was concluded that the lowered intraocular pressure and lowered outflow pressure were the result of a reduction of aqueous inflow. There was no unequivocal experimental demonstration of supersensitization to topical norepinephrine or isoproterenol following chemical sympathetic denervation; however, the experiments were not conclusive on this important point. It was concluded that chemical sympathectomy with 6-hydroxy-dopamine reproduces many of the ocular phenomena of surgical sympathectomy. 6-Hydroxy-dopamine is a useful drug for experimental ophthalmology, and may be useful clinically.
(Investigative Ophthalmology and Visual Science. 1971;10:120-143.)
© 1971 by The Association for Research in Vision and Ophthalmology, Inc.
Chemical sympathectomy disrupts the only known neural input to the pineal gland
- The Pineal Gland: A Pacemaker within the Circadian System of the House Sparrow
- Proceedings of the National Academy of Sciences of the United States of America, Vol. 76, No. 2 (Feb., 1979), pp. 999-1003 (article consists of 5 pages)
Pacemaker after T2 Sympathectomy
Bradycardia and Permanent Pacing After Bilateral Thoracoscopic T2-Sympathectomy for Primary Hyperhidrosis
A 23-year-old woman with craniofacial hyperhidrosis underwent bilateral thoracoscopic T2-sympathectomy. Marked sinus bradycardia with a mean heart rate of 49 beats/min by Holter ECG monitoring occurred after the procedure and persisted for > 2 years. Normal sinus node function was found by an invasive electrophysiological study and unopposed vagotonia after sympathectomy was diagnosed. A permanent pacemaker was implanted. Although reduced heart rate is a common phenomenon after bilateral dorsal sympathectomy, intractable bradycardia with permanent pacing is rare. This patient demonstrates one of the potential cardiac complications of bilateral sympathectomy.Pacing and Clinical Electrophysiology
Volume 24 Issue 4 Page 524-525, April 2001
Can Sympathectomy for Hyperhidrosis be classified as "cure" of hyperhidrosis
Sympathectomy in the case of (for example) Palmar HH exchanges a benign (although understandably uncomfortable condition) for an often disabling, uncontrollable (and more distressing than the original condition) full body sweating, that in some cases requires full clothes change 3 times a day. Patients after the surgery are unable to continue their life as they lived it before the operation. The psychological costs are high, and there have been reported suicides among patients who were struggling with the side-effects. The most recent one in Sydney, Australia.
Which part of this surgery can be called 'treatment' or 'cure'? What is the definition of a 'cure''?
Which part of this surgery can be called 'treatment' or 'cure'? What is the definition of a 'cure''?
Literature - summary
| Wettervik C, Claes G, Drott C, Emanuelsson H, Lomsky M, Rådberg G et al. Endoscopic transthoracic sympathectomy for severe angina. Lancet 1995; 345: 97 - 8. | |
| 3. | Matsumoto Y, Ueyama T, Endo M, Sasaki H, Kasashima F, Abe Y et al. Endoscopic thoracic sympathectomy for Raynaud’s phenomenon. J Vasc Surg 2002; 36: 57 - 61. |
| 4. | Flørenes T. Torakoskopisk sympatektomi - operasjon for håndsvette og ansiktsrødming Tidsskr Nor Lægeforen 2003; 123: 463 - 4. |
| 5. | Drott C, Claes G, Rex L, Dalman P, Gothberg G, Fahlen T. Långtidsresultat efter operation mot handsvett och ansiktsrodnad. Patienterna nöyda trots besvärande biverkningar. Läkartidningen 2001; 98: 1766 - 72. |
| 6. | Telaranta T. Reversal surgery for reducing the side effects of ETS. (SIC!) A case report. Ann Chir Gynaecol 2001; 90: 175 - 6. |
| 7. | Furlan AD, Mailis A, Papagapiou M. Are we paying a high price for surgical sympathectomy? A systematic literature review of late complications. J Pain 2000; 1: 245 - 57. |
| 8. | Abraham P, Picquet J, Bickert S, Papon X, Jousset Y, Saumet J et al. Infra-stellate upper thoracic sympathectomy results in a relative bradychardia during exercise, irrespective of the operated side. Eur J Cardiothorac Surg 2001; 20: 1095 - 100. |
| 9. | DRUMMOND PD. A caution about surgical treatment for facial blushing. Br J Dermatol 2000; 142: 194 - 5. |
Sympathectomy induces adrenergic excitability of cutaneous
Bossut DF, Shea VK, Perl ER.
Sympathectomy induces adrenergic excitability of cutaneous
C-fiber nociceptors.
J Neurophysiol 1996;75:514-7.
Sympathectomy induces adrenergic excitability of cutaneous
C-fiber nociceptors.
J Neurophysiol 1996;75:514-7.
Degeneration patterns of postganglionic fibers following sympathectomy.
Andres KH, Düring M von, Jänig W, Schmidt RF (1985)
Degeneration patterns of postganglionic fibers following sympathectomy.
Anat Embryol 172:133-143
Degeneration patterns of postganglionic fibers following sympathectomy.
Anat Embryol 172:133-143
Denervation Supersensitivity
Neurology 2003;60:1770-1776
© 2003 American Academy of Neurology
C. H. Schick, MD , K. Fronek , A. Held , F. Birklein, MD , W. Hohenberger, MD and M. Schmelz, MD
Before surgery, rewarming kinetics was significantly slower in the patients (n = 61) than in the healthy control subjects (n = 28). Two days after the block, baseline skin temperature increased by about 5 °C, and rewarming was massively accelerated in each of the patients. Three months postoperatively, rewarming kinetics was still accelerated in 36 hands, was unchanged from the preoperative condition in 42, and had worsened in 12. These changes were accompanied by parallel alterations of laser–Doppler flux.
Recurrent and enhanced vasoconstrictor function 3 months following endoscopic sympathetic block has major implications for its use to treat enhanced vasoconstriction.
© 2003 American Academy of Neurology
Differential effects of surgical sympathetic block on sudomotor and vasoconstrictor function
Before surgery, rewarming kinetics was significantly slower in the patients (n = 61) than in the healthy control subjects (n = 28). Two days after the block, baseline skin temperature increased by about 5 °C, and rewarming was massively accelerated in each of the patients. Three months postoperatively, rewarming kinetics was still accelerated in 36 hands, was unchanged from the preoperative condition in 42, and had worsened in 12. These changes were accompanied by parallel alterations of laser–Doppler flux.
Recurrent and enhanced vasoconstrictor function 3 months following endoscopic sympathetic block has major implications for its use to treat enhanced vasoconstriction.
Predicting changes in the distribution of sweating following thoracoscopic sympathectomy
Predicting changes in the distribution of sweating following thoracoscopic sympathectomy
Authors: ANDREWS B.T.1; RENNIE J.A.1, *
Source: British Journal of Surgery, Volume 84, Number 12, December 1997 , pp. 1702-1704(3)
Publisher: John Wiley & Sons, Ltd.
Abstract:
Background Compensatory sweating is a common symptom following thoracic sympathectomy; however, the reported incidence of this complication varies greatly, and its severity has not been quantified.
Methods In this study changes in the distribution of sweating following bilateral T2-3 thoracoscopic sympathectomy for hyperhidrosis were assessed in 42 patients. Sweat production in the palms, axillae, face, trunk and feet was assessed using a linear analogue scale.
Results The operation was most successful in reducing sweat production in the palms, axillae and face (in descending order). The operation also reduced pedal sweat production in 12 of the 29 patients who suffered concomitant pedal hyperhidrosis. Compensatory truncal sweating occurred in 36 of the 42 patients; it was severe in ten, moderate in 16 and minimal in ten.
Conclusion Patients should be warned about compensatory sweating before thoracic sympathectomy.
Sunday, April 13, 2008
Postoperative Autonomic Deficit
BACKGROUND: Upper thoracic sympathectomy is used to treat several disorders. Sympathetic nerve fibers emanating from thoracic ganglia innervate the heart. Whether unilateral or bilateral upper thoracic sympathectomy affects cardiac sympathetic innervation in humans in vivo has been unclear. OBJECTIVES: The purpose of this study was to assess whether thoracic sympathectomy decreases cardiac sympathetic innervation, as indicated by positron emission tomographic scanning after intravenous injection of the sympathoneural imaging agent 6-[18F]fluorodopamine. METHODS: Nine patients with previous upper thoracic sympathectomies (four right-sided, one left-sided, four bilateral) underwent thoracic 6-[18F]fluorodopamine scanning between 1 and 2 hours after injection of the imaging agent. In each case, a low rate of entry of norepinephrine into the arm venous drainage (norepinephrine spillover) verified upper limb sympathectomy. Data were compared with those from the interventricular septum of patients with cardiac sympathetic denervation associated with pure autonomic failure and from normal volunteers. RESULTS: All four patients with bilateral sympathectomy had low septal myocardial 6-[18F]fluorodopamine-derived radioactivity (2,673 +/- 92 nCi-kg/cc-mCi at an average of 89 minutes after injection) compared with normal volunteers (3,634 +/- 311 nCi-kg/cc-mCi at 83 minutes, N = 22, P = .007) and higher radioactivity than in patients with pure autonomic failure (1,320 +/- 300 nCi-kg/cc-mCi at 83 minutes, N = 7, P = .003). Patients with unilateral sympathectomy had normal 6-[18F]fluorodopamine-derived radioactivity (3,971 +/- 337 nCi-kg/cc-mCi at 87 minutes). CONCLUSIONS: Bilateral upper thoracic sympathectomy partly decreases cardiac sympathetic innervation density.
Aberrant regeneration following sympathectomy - Frey's Syndrome
Physiological gustatory facial sweating and flushing commonly occur in response to eating spicy foods containing capsacin. This response, combined with salivation, lacrimation, and nasal secretion occurs more easily in warm climates where sweat glands are already at a subthreshold level of excitaiton for thermal sweating (Lee 1954).
The pattern is symmetrical with sweating involving the head and exceptionally the neck, and with flushing most apparent in the nose and cheek (Haxton 1948; Monro 1959, Fox et al. 1962; Drummond and Lance 1987).
Aberrant regeneration following sympathectomy can give rise to pathological gustatory facial flushing and sweating. Weeks, months, or years after cervicothoracic preganglionic sympathectomy, gustatory sweating and flushing may develop on the denervated side along with impaired thermoregulatory sweating. (Bloor 1969; Kurchin at al. 1977)
Sympathetic preganglionic fibers originally destined for the salivary glands may be responsible through faulty reinnervation of the stellate ganglion... (Bloor, 1969; Drummond and Lance 1987).
Interruption of postganglionic sympathetic facial fibers may render residual neurilemmal sheaths and sympathetic endings susceptible to stray collateral sprouting or faulty regeneration of parasympathetic fibers that normally mediate salivation.
The pattern is symmetrical with sweating involving the head and exceptionally the neck, and with flushing most apparent in the nose and cheek (Haxton 1948; Monro 1959, Fox et al. 1962; Drummond and Lance 1987).
Aberrant regeneration following sympathectomy can give rise to pathological gustatory facial flushing and sweating. Weeks, months, or years after cervicothoracic preganglionic sympathectomy, gustatory sweating and flushing may develop on the denervated side along with impaired thermoregulatory sweating. (Bloor 1969; Kurchin at al. 1977)
Sympathetic preganglionic fibers originally destined for the salivary glands may be responsible through faulty reinnervation of the stellate ganglion... (Bloor, 1969; Drummond and Lance 1987).
Interruption of postganglionic sympathetic facial fibers may render residual neurilemmal sheaths and sympathetic endings susceptible to stray collateral sprouting or faulty regeneration of parasympathetic fibers that normally mediate salivation.
Pathological gustatory sweating and flushing can develop
after injury to preganglionic cervicothoracie sympathetic fibres, an
unavoidable consequence of resecting that part of the sympathetic chain. The
mechanism of this abnormal response is uncertain; conceivably, though,
regeneration of injured salivatory fibres or collateral sprouting from nearby
intact fibres creates aberrant connections between salivatory fibres and
denervated vasomotor and sudomotor neurons in the superior cervical ganglion. 7
Commands to salivate would then be translated into commands to sweat and flush
in the distribution of sympathetic denervation. Cross-innervation lower down in
the stellate ganglion can also produce unusual and potentially distressing
autonomic disturbances in the sympathetically denervated arm (e.g.
piloerection while eating)
P.D.DRUMMOND
School of Psychology, Murdoch University,
South Street, Murdoch,
Chronic Idiopathic Anhidrosis - Consequence of Sympathectomy
Chronic Idiopathic Anhidrosis is a syndrome of unknown etiology - a heat intolerance that correlates with generalized or regional sweating defects.
gustatory sweating occurred in 32% of patients
The questionnaire was returned by 96% of patients after a median of 17 months. 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.
Gustatory Side Effects After Thoracoscopic Sympathectomy
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T11-4J963XN-1R&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=7cad987402b12485375284dc221ec19b
NE Loss Causes Motor Impairment
Norepinephrine loss produces more profound motor deficits than MPTP treatment in mice
Departments of *Human Genetics and Environmental and Occupational Health, Rollins School of Public Health, Emory University, Atlanta, GA 30322; and Department of Physiology and Pharmacology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602
Edited by Richard D. Palmiter, University of Washington School of Medicine, Seattle, WA, and approved June 25, 2007 (received for review March 27, 2007)
http://www.pnas.org/cgi/content/full/104/34/13804
NE Loss Causes Motor Impairment. We suggest two possible mechanisms for the motor impairments of Dbh–/– and LC-lesioned mice. SI Fig. 6).
Depression of T cell immunity following chemical sympathectomy
Alterations in Sympathetic Noradrenergic Innervation in Lymphoid ...
Sympathetic neural modulation of the immune system. I. Depression of T cell immunity in vivo and in vitro following chemical sympathectomy. Brain Behav. ...www.annalsnyas.org/cgi/content/full/840/1/262
depletion of brain noradrenaline levels causes a disturbance in cerebral microvascular tone
| Thirty male Wistar rats, weighing 350 to 400 gm each, received stereotactic injections of 6-hydroxydopamine (300 micrograms/kg) into the left lateral ventricle. The same amount of saline was injected into a control group of 15 rats. Seven days after this procedure, cerebral blood flow (CBF) was measured by the hydrogen clearance method. A hypertensive condition at a mean arterial pressure of about 160 mm Hg was maintained for 1 hour by intravenous infusion of phenylephrine. In the 6-hydroxydopamine-treated group, CBF increased significantly after the elevation of systemic blood pressure compared with that in the control group, and cerebral autoregulation was impaired. After a 1-hour study, the specific gravity of the cerebral tissue in the treated group significantly decreased; electron microscopic studies at that time revealed brain edema. It is suggested that depletion of brain noradrenaline levels causes a disturbance in cerebral microvascular tone and renders the cerebral blood vessels more vulnerable to hypertension. | |
| Authors | H Kobayashi, M Hayashi, H Kawano, Y Handa, M Kabuto, H Ide (Affiliation: Department of Neurosurgery, Fukui Medical School, Matsuoka, Japan.) |
|---|---|
| Journal | Journal of neurosurgery (J Neurosurg) Vol. 75 Issue 6 Pg. 906-10 (Dec 1991) ISSN: 0022-3085 UNITED STATES |
| PMID | 1941119 (Publication Type: Journal Article) |
American Institute for Hyperhidrosis claims to cure anxiety and palpitations with ETS
Palpitations caused by anxiety can be significantly reduced.
Migraine occurrence and trembling of the hands may improve.
(They also claim, that Copensatory Hyperhidorsis is) "tolerable by most patients and only 5% describe it as troublesome. Some patients say it improves with time."
http://www.handsweat.com/sideeff.html
Question: what is the scientific definition for troublesome? Some patients say it improves with time? Surely that is not a statement worthy of a website such as this.
There has been no clinical evaluation of the severity of the so called CS to this day. Surgeons who perform the surgery and profit from it claim it to be close to insignificant..that even improves with time. Other sources will state 90% of severe CS, and 25% disabling CS. Surely it can not be just a question of semantics when you have a 25% chance of being disabled after an elective surgery!
Doctors are unable to support their claims about the positive outcomes of the surgery. There has been no controlled trial to support their positive advertising, and it is left solely to the discretion of the surgeon to admit or deny the incidence and severity of the side-effects.
Migraine occurrence and trembling of the hands may improve.
(They also claim, that Copensatory Hyperhidorsis is) "tolerable by most patients and only 5% describe it as troublesome. Some patients say it improves with time."
http://www.handsweat.com/sideeff.html
Question: what is the scientific definition for troublesome? Some patients say it improves with time? Surely that is not a statement worthy of a website such as this.
There has been no clinical evaluation of the severity of the so called CS to this day. Surgeons who perform the surgery and profit from it claim it to be close to insignificant..that even improves with time. Other sources will state 90% of severe CS, and 25% disabling CS. Surely it can not be just a question of semantics when you have a 25% chance of being disabled after an elective surgery!
Doctors are unable to support their claims about the positive outcomes of the surgery. There has been no controlled trial to support their positive advertising, and it is left solely to the discretion of the surgeon to admit or deny the incidence and severity of the side-effects.
Sympathectomy leads to a decrease in noradrenaline levels in the cerebral cortex
Chemical Sympathectomy leads to a decrease in noradrenaline levels measured in the cerebral cortex. (Onesti at al. 1989)
brain levels of norepinephrine were reduced significantly
EFFECT OF 6-HYDROXYDOPAMINE ON BRAIN NOREPINEPHRINE AND DOPAMINE: EVIDENCE FOR SELECTIVE DEGENERATION OF CATECHOLAMINE NEURONS
1 Departments of Psychiatry and Pharmacology and the Child Development Institute, University of North Carolina School of Medicine, Chapel Hill, North Carolina
After the intracisternal administration of 6-hydroxydopamine, brain levels of norepinephrine were reduced significantly with or without pargyline pretreatment. Depletion of dopamine in the central nervous system was found to be enhanced markedly by pargyline administration at higher dose levels of 6-hydroxydopamine. Brain serotonin concentrations were not altered. The effects of 6-hydroxydopamine were long-lasting with the depletion of brain amines persisting at 78 days. After norepinephrine-H3 intracisternally to animals treated with 6-hydroxydopamine, labeled norepinephrine uptake was diminished with a corresponding reduction of deaminated catechols and a marked increased in methylated amines. Tyrosine hydroxylase activity was found to be reduced in brainstem, caudate nucleus and whole brain in 6-hydroxydopamine-treated animals. Conversion of tyrosine-H3 to labeled norepinephrine and dopamine was also markedly diminished. The results support the view that 6-hydroxydopamine produces a "central sympathectomy" when introduced into cerebrospinal fluid.
Journal of Pharmacology And Experimental Therapeutics, Vol. 174, Issue 3, 413-420, 1970Copyright © 1970 by American Society for Pharmacology and Experimental Therapeutics
6-OHDA depressed hypothalamic norepinephrine levels in both sexes
6-OHDA depressed hypothalamic norepinephrine levels in both sexes.
Copyright © 1973 S. Karger AG, Basel
Copyright © 1973 S. Karger AG, Basel
Sex-Dependent Increase in Pineal Hydroxyindole-O-Methyl Transferase Activity After a Single Intraventricular Injection of 6-Hydroxydopamine to Newborn Rats
M.T. Hyyppä, D.P. Cardinali, R.J. Wurtman
Laboratory of Neuroendocrine Regulation, Department of Nutrition and Food Science, Massachusetts Institute of Technology, Cambridge, Massachusetts
Neuroendocrinology 1973;11:274-283 (DOI: 10.1159/000122140)
sympathectomy impairing adrenergic transmission
The chronic bilateral cervical superior sympathectomy could provoke norepinephrine depletion in the small granular vesicles of the sympathetic terminals, impairing adrenergic transmission; this would then eliminate the constrictor sympathetic effect13. Our study is in agreement with published data where pharmacological or anatomical exclusion of the sympathetic activity prevented vasospasm24.
Antônio Tadeu de Souza FaleirosI; Francisco Humberto de Abreu MaffeiII; Luiz Antonio de Lima ResendeIII
IServices of Neurosurgery, Botucatu School of Medicine, São Paulo State University (UNESP), Botucatu, SP, Brazil
IIVascular Surgery, Botucatu School of Medicine, São Paulo State University (UNESP), Botucatu, SP, Brazil
IIINeurology, Botucatu School of Medicine, São Paulo State University (UNESP), Botucatu, SP, Brazil
marked changes in brain NE following sympathectomy
Biochemical and functional evaluation of the sympathectomy produced by the administration of guanethidine to newborn rats
EM Johnson , E Cantor and JR Douglas
The administration of guanethidine to newborn rats has been shown by morphological criteria to destroy sympathetic neurons. Newborn rats were injected with guanethidine (50-100 mg/kg/day for 20 days). Upon maturation (at 10 weeks old), the degree of destruction of the sympathetic nervous system (sympathectomy) was assessed. Marked decreases (80-98%) in the norepinephrine concentration in several tissues (heart, spleen, intestine, mesentery, kidney, uterus, vas deferens) were observed in the guanethidine-treated rats when compared to saline-treated controls. No changes were observed in the epinephrine concentration in the adrenals or in the norepinephrine levels in whole brain. Analysis of brain areas showed no change in the norepinephrine levels in brain stem and cerebrum and a small (18%) decrease in the cerebellum. Stimulation of the sympathetic vasomotor outflow in the pithed rat preparation produced almost no response in guanethidine- treated animals. Periarterial nerve stimulation of the isolated perfused kidney preparation also produced essentially no response in guanethidine-treated animals. Isolated intestinal preparations from guanethidine-treated animals responded to nerve stimulation with contractions rather than relaxation as seen in preparations from control animals. Isolated vas deferens preparations responded normally to nerve stimulation despite a 95% decrease in tissue norepinephrine concentration. These data indicate that administration of guanethidine to newborn rats produces a more complete peripheral sympathectomy, especially of the vasculature, than immunosympathectomy or neonatal administration of 6-hydroxydopamine and does so with no significant effect on central noradrenergic neurons.
Volume 193, Issue 2, pp. 503-512, 05/01/1975
Copyright © 1975 by American Society for Pharmacology and Experimental Therapeutics
the adrenergic system in regulation of the metabolism of the retina
Stefan M. Pojda1 
and Ryszard Brus2
| (1) | Department of Ophthalmology, Silesian Academy of Medicine, Francuska str. 20/24, 40-027 Katowice, Poland |
| (2) | Department of Pharmacology, Silesian Academy of Medicine, Zabrze 8, Poland |
Received: 16 April 1976
Summary Male Wistar rats were injected intraventricularly with two doses of 250 mcg of 6-hydroxydopamine (6-OHDA) in two consecutive days. Two weeks later the oxygen uptake, anaerobic glycolysis and lactic acid dehydrogenase (LDH) activity in the retina were determined. The decrease of oxygen uptake (–28 %), anaerobic glycolysis (–31 %) and LDH activity (–12 %) in rats treated with 6-OHDA in comparison to control animals was found. The possible role of the adrenergic system in regulation of the metabolism of the retina is discussed.
Heightened emotions cause experiences to crystallize into lasting and vivid memories
Emotional memory.(NEUROSCIENCE)(effect of Norepinephrine to memory)(Brief article)
Where were you on Sept. 11, 20017 Or when the shuttle Challenger exploded in 19867 Heightened emotions cause experiences to crystallize into lasting and vivid memories. This boost in memory formation is due in part to the stress hormone norepinephrine, but scientists haven't understood how the hormone causes this effect.
Now researchers have uncovered molecular changes triggered by norepinephrine that help nerve cells form new memories.
A team led by Roberto Malinow of Cold Spring Harbor Laboratory in New York traced the hormone's effects to a receptor molecule called glutamate receptor 1 (G1uR1) on the surfaces of nerve cells. Through G1uR1 and similar receptors, ... http://www.highbeam.com/doc/1G1-170372501.html
brain norepinephrine turnover, and memory and the need for Power
David C. McClelland1 , J. Anderson Maddocks1 and Dan P. McAdams1, 2
| (1) | Department of Psychology and Social Relations, Harvard University, 33 Kirkland Street, 02138 Cambridge, Massachusetts |
| (2) | Present address: Loyola University of Chicago, USA |
Abstract Subjects were classified according to whether they were high or low in the need for Power and high or low in gain in 3-methoxy-4-hydroxyphenylglycol (MHPG), a putative index of brain norepinephrine (NE) turnover, after engaging in some tasks that involved memory for story content. Subjects who were high inn Power and in the index of brain NE turnover showed better recall of power-related facts than subjects low on both these characteristics, confirming an earlier finding, which suggests that the need for Power is subserved by a noradrenergic reward system in the brain.
The need for power, brain norepinephrine turnover, and memory
| Journal | Motivation and Emotion |
| Publisher | Springer Netherlands |
| ISSN | 0146-7239 (Print) 1573-6644 (Online) |
| Issue | Volume 9, Number 1 / March, 1985 |
| DOI | 10.1007/BF00991546 |
| Pages | 1-10 |
| Subject Collection | Behavioral Science |
| SpringerLink Date | Monday, January 10, 2005 |
Norepinephrine
Doze said the adrenergic system — one of the essential neurochemical systems in the brain — synthesizes and controls the release of the neurotransmitter norepinephrine (also known as noradrenalin).
Norepinephrine works in both the central and peripheral nervous systems. It’s responsible for many critical functions, but in this context, its key functions in the central nervous system include sleep, emotions, learning, and memory.Probing the deepest levels of brain chemistry to uncover clues to memory loss
By Juan Miguel Pedraza
Emotion enhances learning via norepinephrine regulation
A neurotransmitter involved in emotional arousal enhances learning by phosphorylating glutamate receptors.
Do you remember the song that was playing during your first kiss? Both positive and negative emotions influence learning and memory but researchers have not determined the mechanism. Now Hu et al. report that the neurotransmitter norepinephrine regulates glutamate receptor trafficking in a recent article in Cell.
Axon terminals containing norepinephrine synapse in the hippocampus and amygdala, which are important in emotional memory. In the hippocampus, norepinephrine reduces the threshold for long-term potentiation (LTP), which is thought to be a substrate of memory. Norepinephrine acts at 
-adrenergic receptors, where it activates cAMP-dependent protein kinase (PKA) and calcium/calmodulin-dependent protein kinase II (CaMKII). These kinases phosphorylate serines 845 and 831, respectively, in the AMPA glutamate receptor type 1 (GluR1). The authors proposed that norepinephrine regulates learning by phosphorylating AMPA receptors.
Hu, H. et al. Emotion enhances learning via norepinephrine regulation of AMPA-receptor trafficking. Cell 131, 160–173 (2007). | Article | PubMed |
Emotional intelligence
Neuroscience Gateway (October 2007) |
The excitatory actions of epinephrine were not observed
The excitatory actions of epinephrine were not observed in groups given an identical dose of the hormone after peripheral β-adrenergic receptor blockade with sotalol. These findings demonstrate that neural discharge in vagal afferent fibers is increased by elevations in peripheral concentrations of epinephrine and the significance of these findings in understanding how epinephrine modulates brain limbic structures to encode and store new information into memory is discussed.
Received 9 June 2005;
Epinephrine administration increases neural impulses propagated along the vagus nerve: Role of peripheral β-adrenergic receptors
Received 9 June 2005;
revised 17 August 2005;
accepted 29 August 2005.
Available online 17 October 2005.
arousal related hormone affects memory processing
A significant number of animal and human studies demonstrate that memories for new experiences are encoded more effectively under environmental or laboratory conditions which elevate peripheral concentrations of the hormone epinephrine and in turn, induce emotional arousal. Although this phenomenon has been replicated across several learning paradigms, understanding of how this arousal related hormone affects memory processing remains obscure because epinephrine does not freely enter into the central circulation to produce any direct effects on the brain. This study examined whether epinephrine’s actions on the CNS may be mediated by the initial activation of peripheral vagal fibers that project to the brain.
Received 9 June 2005;
Epinephrine administration increases neural impulses propagated along the vagus nerve: Role of peripheral β-adrenergic receptors
Received 9 June 2005;
revised 17 August 2005;
accepted 29 August 2005.
Available online 17 October 2005.
The role of norepinephrine in spatial reference and spatial working memory
The role of norepinephrine in spatial reference and spatial working memory
The adrenergic system (utilizing norepinephrine, NE, as a neurotransmitter) is implicated in hippocampus-based learning and memory, in addition to its well known peripheral actions mediated by the sympathetic nervous system.
Michael J. Gertner, University of Pennsylvania
Steven A. Thomas, University of Pennsylvania
The adrenergic system (utilizing norepinephrine, NE, as a neurotransmitter) is implicated in hippocampus-based learning and memory, in addition to its well known peripheral actions mediated by the sympathetic nervous system.
Michael J. Gertner, University of Pennsylvania
Steven A. Thomas, University of Pennsylvania
Norepinephrine Important In Retrieving Memories
Norepinephrine Important In Retrieving Memories
Source: U. Of Pennsylvania Medical Center
Date: 2 April 2004
In addition, beta-blockers, which are used to treat heart failure and hypertension (among other ailments) block the same norepinephrine receptors important for memory retrieval. Therefore, when treating heart disease, the use of beta blockers that do not cross into the brain may help to avoid memory-related side effects, suggest the researchers.
The findings of this research appear in the April 2 issue of Cell.
Source: U. Of Pennsylvania Medical Center
Date: 2 April 2004
In addition, beta-blockers, which are used to treat heart failure and hypertension (among other ailments) block the same norepinephrine receptors important for memory retrieval. Therefore, when treating heart disease, the use of beta blockers that do not cross into the brain may help to avoid memory-related side effects, suggest the researchers.
The findings of this research appear in the April 2 issue of Cell.
Causes of Orthostatic Hypotension
Causes of Orthostatic Hypotension:
Neurologic (involving autonomic dysfunction)
Surgical sympathectomy
http://www.merck.com/mmpe/sec07/ch069/ch069d.html
Neurologic (involving autonomic dysfunction)
Surgical sympathectomy
http://www.merck.com/mmpe/sec07/ch069/ch069d.html
NE levels and Posttraumatic Stress Disorder
CSF Norepinephrine Concentrations in Posttraumatic Stress Disorder
Thomas D. Geracioti, Jr., M.D.
Dewleen G. Baker, M.D.
Nosakhare N. Ekhator, M.S.
Scott A. West, M.D.
Kelly K. Hill, M.D.
Ann B. Bruce, M.D.
Dennis Schmidt, Ph.D.
Barbara Rounds-Kugler, R.N.
Rachel Yehuda, Ph.D.
Paul E. Keck, Jr., M.D.
John W. Kasckow, M.D., Ph.D.
Objective: Despite evidence of hyperresponsive peripheral and central nervous system (CNS) noradrenergic activity in posttraumatic stress disorder (PTSD), direct measures of CNS norepinephrine in PTSD have been lacking. The goal of this study was to determine serial CSF norepinephrine levels in patients with PTSD.
Method: CSF samples were obtained serially over a 6-hour period in 11 male combat veterans with chronic PTSD and eight healthy men through an indwelling subarachnoid catheter. Thus the authors were able to determine hourly CSF norepinephrine concentrations under base-
line (unstressed) conditions. Severity of the patients’ PTSD symptoms was assessed with the Clinician-Administered PTSD Scale.
Results: CSF norepinephrine concentrations were significantly higher in the men
with PTSD than in the healthy men. Moreover, CSF norepinephrine levels strongly and
positively correlated with the severity of PTSD symptoms. Plasma norepinephrine concentrations showed no significant relationship with the severity of PTSD symptoms.
Conclusions: These findings reveal the presence of greater CNS noradrenergic activity under baseline conditions in patients with chronic PTSD than in healthy subjects and directly link this pathophysiologic observation with the severity of the clinical posttraumatic stress syndrome.
(Am J Psychiatry 2001; 158:1227–1230)
Thomas D. Geracioti, Jr., M.D.
Dewleen G. Baker, M.D.
Nosakhare N. Ekhator, M.S.
Scott A. West, M.D.
Kelly K. Hill, M.D.
Ann B. Bruce, M.D.
Dennis Schmidt, Ph.D.
Barbara Rounds-Kugler, R.N.
Rachel Yehuda, Ph.D.
Paul E. Keck, Jr., M.D.
John W. Kasckow, M.D., Ph.D.
Objective: Despite evidence of hyperresponsive peripheral and central nervous system (CNS) noradrenergic activity in posttraumatic stress disorder (PTSD), direct measures of CNS norepinephrine in PTSD have been lacking. The goal of this study was to determine serial CSF norepinephrine levels in patients with PTSD.
Method: CSF samples were obtained serially over a 6-hour period in 11 male combat veterans with chronic PTSD and eight healthy men through an indwelling subarachnoid catheter. Thus the authors were able to determine hourly CSF norepinephrine concentrations under base-
line (unstressed) conditions. Severity of the patients’ PTSD symptoms was assessed with the Clinician-Administered PTSD Scale.
Results: CSF norepinephrine concentrations were significantly higher in the men
with PTSD than in the healthy men. Moreover, CSF norepinephrine levels strongly and
positively correlated with the severity of PTSD symptoms. Plasma norepinephrine concentrations showed no significant relationship with the severity of PTSD symptoms.
Conclusions: These findings reveal the presence of greater CNS noradrenergic activity under baseline conditions in patients with chronic PTSD than in healthy subjects and directly link this pathophysiologic observation with the severity of the clinical posttraumatic stress syndrome.
(Am J Psychiatry 2001; 158:1227–1230)
Alterations in T and B cell proliferation and differentiation in vitro following chemical sympathectomy
Madden, K.S., Moynihan, J.A., Brenner, G.J., Felten, S.Y., Felten, D.L. and Livnat, S. (1994b).:Sympathetic nervous system modulation of the immune system. III. Alterations in T and B cell proliferation and differentiation in vitro following chemical sympathectomy. J. Neuroimmunol. 49: 77-87.
reduced antibody responses to T-dependent antigens
It has been exhaustively demonstrated that the regions in which lymphocytes T cells reside, and through which they recirculate, receive direct sympathetic neural input. Therefore, the immune system can be considered “hard-wired” to the brain. Chemical sympathectomy of adult mice resulted in reduced antibody responses to T-dependent antigens. The interaction between sympathetic NA nerve fibers and cells of the immune system has been shown through the distribution of tyrosine hydrolase (TH+) nerve fibers among lymphocytes and macrophages in lymphoid organs, the expression of adrenoceptors on cells of the immune system, and the immunomodulatory effects of NA. In old rats, a conspicuous decline in NA innervation and NA contents is observed in the splenic white pulp as well as in the cell bodies in superior celiac-mesenteric ganglia that provide preganglionic sympathetic innervation to the spleen (Arnason, 1993; Carlson, Fox et al., 1997; Madden. Felten et al., 1994a; Roszman and Carlson, 1991). Paralleling these alterations in sympathetic NA neuronal activity is an age-related loss of T cell mediated immune responses, including reduced T cell proliferation and IL-2 production by antigen- and mitogen-stimulated lymphocytes. Treatment of these rats with drugs inducing noradrenergic regeneration and re-innervation reverted the rats’ immune abnormalities (Tang, Shankar et al., 1999; Thyaga-Rajan, Madden et al., 1999). Noradrenergic innervation of the spleen is responsible for a significant increase of gamma-interferon, IL-2 and tumor necrosis factor alpha, the three Th-1 cytokines, and a lowering of IL-4, IL-5 and IL-10 (TH-2 cytokines) production (Carlson, Fox et al., 1997; Madden, Moynihan et al., 1994b; Spengler, Allen et al., 1990). Other evidence showed that elevated plasma NA concentrations increased the level of Th-1 cytokines (Kappel, Poulsen et al., 1998; Ross, Williams et al., 1987). These and other findings demonstrate that the noradrenergic innervation of bone marrow is functionally dynamic and is responsive to central activation. Furthermore, these results lend credence to the premise that neural mechanisms participate in regulating lymphopoietic cellular events.
VOL. 31, NOS. 5 & 6, 2000 JOURNAL OF MEDICINE
JOURNAL OF MEDICINE
Copyright © 2000 by
PJD Publications Limited
The hepatic sympathetic nerve
Mortality in sympathectomised mice was significantly higher than that in sham operated mice following administration of Jo-2. This result was also supported by apoptosis data in which sympathectomised livers exhibited a significant elevation in the number of apoptotic hepatocytes and caspase-3 activity after Jo-2 treatment compared with sham operated livers. Moreover, pretreatment with norepinephrine dose dependently inhibited the hepatic sympathectomy induced increase in mortality after Jo-2 injection. Antiapoptotic protein levels of FLICE inhibitory protein, Bcl-xL, and Bcl-2 in the liver were significantly lower in sympathectomised mice at one and two hours following Jo-2 treatment than in sham operated animals. In addition, interleukin 6 supplementation dose dependently suppressed the hepatic sympathectomy induced increase in mortality after Jo-2 treatment.
Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
The hepatic sympathetic nerve plays a critical role in preventing Fas induced liver injury in mice
Y Chida1, N Sudo1, A Takaki2, C Kubo1 1 Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan
2 Department of Integrative Physiology, Graduate School of Medical Sciences, Kyushu University, Higashi-ku, Fukuoka, Japan
Dr Y Chida
Department of Psychosomatic Medicine, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan
The sympathoadrenal system is one of the major pathways mediating physiological responses
The sympathoadrenal system is one of the major pathways mediating physiological responses in the organism. The sympathoadrenal system plays an important role in the regulation of blood pressure, glucose, sodium and other key physiological and metabolic processes. In many disease states, the sympathoadrenal system is affected and by corrective physiological responses the sympathoadrenal system preserves homeostasis. Many therapeutic agents are either adrenergic activators or inhibitors. Therefore, measurements of the components of the sympathoadrenal system and the activity of the sympathoadrenal system have been of major interest for decades.
Levels of plasma (p-) noradrenaline (NA), the sympathetic neurotransmitter, have been used to indicate activity of the neuronal sympathoadrenal component, while adrenaline (Adr) levels indicate activity of the hormonal adrenomedullary component of the sympathoadrenal system (Christensen 1991, Goldstein 1995, Christensen & Norsk 2000). Based upon the absence of an arterio-venous increase in p-DOPA concentration in sympathectomized limbs and a decrease in p-DOPA after inhibition of tyrosine hydroxylase (TH) in dogs, it was concluded that DOPA can pass across sympathetic neuronal membranes to reach the general circulation and furthermore, that p-DOPA may be related to regional rate of tyrosine hydroxylation (Goldstein et al 1987a). P-DOPA only demonstrated minimal changes during stimuli that produced significant changes in p-NA. Due to partly parallel changes of p-NA and p-DOPA, however, it was believed that p-DOPA reflect the rate of catecholamine synthesis and that p-DOPA was a simple and direct index of TH activity in vivo (Eisenhofer et al 1988, Goldstein & Eisenhofer 1988, Garty et al 1989b). It was inferred that p-DOPA levels may be an index of sympathetic activity.
Levels of plasma (p-) noradrenaline (NA), the sympathetic neurotransmitter, have been used to indicate activity of the neuronal sympathoadrenal component, while adrenaline (Adr) levels indicate activity of the hormonal adrenomedullary component of the sympathoadrenal system (Christensen 1991, Goldstein 1995, Christensen & Norsk 2000). Based upon the absence of an arterio-venous increase in p-DOPA concentration in sympathectomized limbs and a decrease in p-DOPA after inhibition of tyrosine hydroxylase (TH) in dogs, it was concluded that DOPA can pass across sympathetic neuronal membranes to reach the general circulation and furthermore, that p-DOPA may be related to regional rate of tyrosine hydroxylation (Goldstein et al 1987a). P-DOPA only demonstrated minimal changes during stimuli that produced significant changes in p-NA. Due to partly parallel changes of p-NA and p-DOPA, however, it was believed that p-DOPA reflect the rate of catecholamine synthesis and that p-DOPA was a simple and direct index of TH activity in vivo (Eisenhofer et al 1988, Goldstein & Eisenhofer 1988, Garty et al 1989b). It was inferred that p-DOPA levels may be an index of sympathetic activity.
Department of Internal Medicine and Endocrinology, Herlev University Hospital, Herlev.
Correspondence: Ebbe Eldrup, Bolbrovænge 29, DK-2960 Rungsted Kyst.
Saturday, April 12, 2008
Sympathectomy - treatment for Long QT Syndrome
The long-term treatment is aimed at reducing the QT-interval duration and preventing the torsades and sudden death and includes use of oral [beta]-adrenergic blockers, implantation of permanent pacemaker/cardioverter-defibrillator, and left thoracic
sympathectomy.
American Heart Journal. 143(1):7-14, January 2002.
Khan, Ijaz A. MD, FACP, FACC
sympathectomy.
American Heart Journal. 143(1):7-14, January 2002.
Khan, Ijaz A. MD, FACP, FACC
Sympathetic blocks can also alter the function of organs that have a sympathetic control component
Sympathetic blocks can also alter the function of organs that have a sympathetic control component...
However, surgical sympathectomy may result in a compensatory hyperhidrosis: a condition characterized by abnormally profuse sweating in a location remote form the sympathectomy. Other complications can also occur, including paresis, paralysis, and bowel or bladder dysfunction. Neurolytic procedures typically can only be considered if all other measures have failed.
http://www.wipo.int/pctdb/en/wo.jsp?IA=WO2005072433&wo=2005072433&DISPLAY=DESC
However, surgical sympathectomy may result in a compensatory hyperhidrosis: a condition characterized by abnormally profuse sweating in a location remote form the sympathectomy. Other complications can also occur, including paresis, paralysis, and bowel or bladder dysfunction. Neurolytic procedures typically can only be considered if all other measures have failed.
http://www.wipo.int/pctdb/en/wo.jsp?IA=WO2005072433&wo=2005072433&DISPLAY=DESC
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