The amount of compensatory sweating depends on the patient, the damage that the white rami communicans incurs, and the amount of cell body reorganization in the spinal cord after surgery.
Other potential complications include inadequate resection of the ganglia, gustatory sweating, pneumothorax, cardiac dysfunction, post-operative pain, and finally Horner’s syndrome secondary to resection of the stellate ganglion.
www.ubcmj.com/pdf/ubcmj_2_1_2010_24-29.pdf

After severing the cervical sympathetic trunk, the cells of the cervical sympathetic ganglion undergo transneuronic degeneration
After severing the sympathetic trunk, the cells of its origin undergo complete disintegration within a year.

http://onlinelibrary.wiley.com/doi/10.1111/j.1439-0442.1967.tb00255.x/abstract

Monday, April 21, 2008

Sympathectomy improves skin blood flow at the thermoregulatory but not the nutritive level

These results indicate that in case of lower limb ischemia, sympathectomy improves skin blood flow at the thermoregulatory but not the nutritive level of skin microcirculation. This may be related to the fact that the thermoregulatory vessels are mainly sympathetically controlled, whereas the nutritive capillaries are mainly controlled by local (nonneural) factors.

François M.H. van Dielen1, Harrie A.J.M. Kurvers1, Ruben Dammers1, Mirjam G.A. oude Egbrink2, Dick W. Slaaf3, Jan H.M. Tordoir1 and Peter J.E.H.M. Kitslaar1

(1) Department of General Surgery, Cardiovascular Research Institute Maastricht and University Hospital Maastricht, PO Box 5800, 6202 AZ Maastricht, The Netherlands, NL
(2) Department of Physiology, Cardiovascular Research Institute Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands, NL
(3) Department of Biophysics, Cardiovascular Research Institute Maastricht, PO Box 616, 6200 MD Maastricht, The Netherlands, NL

World Journal of Surgery Volume 22, Number 8 / August, 1998

Imbalance of regional cerebral blood flow

Imbalance of regional cerebral blood flow and oxygen consumption: effect of vascular alpha adrenoceptor blockade.


Neuropharmacology. 1993 Mar;32(3):297-302.
Weiss HR, Sinha AK.

Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, Piscataway 08854-5635.

the regulation of cerebrovascular tone

Brain perfusion is tightly coupled to neuronal activity, is commonly used to monitor normal or pathological brain function, and is a direct reflection of the interactions that occur between neuronal signals and blood vessels. Cerebral blood vessels at the surface and within the brain are surrounded by nerve fibers that originate, respectively, from peripheral nerve ganglia and intrinsic brain neurons. Although of different origin and targeting distinct vascular beds, these "perivascular nerves" fulfill similar roles related to cerebrovascular functions, a major one being to regulate their tone and, therein, brain perfusion. This utmost function, which underlies the signals used in functional neuroimaging techniques and which can be jeopardized in pathologies such as Alzheimer's disease, stroke, and migraine headache, is thus regulated at several levels. Recently, new insights into our understanding of how neural input regulate cerebrovascular tone resulted in the rediscovery of the functional "neurovascular unit." These remarkable advances suggest that neuron-driven changes in vascular tone result from interactions that involve all components of the neurovascular unit, transducing neuronal signals into vasomotor responses not only through direct interaction between neurons and vessels but also indirectly via the perivascular astrocytes. Neurovascular coupling is thus determined by chemical signals released from activated perivascular nerves and astrocytes that alter vascular tone to locally adjust perfusion to the spatial and temporal changes in brain activity.
Edith Hamel

Laboratory of Cerebrovascular Research, Montreal Neurological Institute, McGill University, Montréal, Québec, Canada

J Appl Physiol 100: 1059-1064, 2006; doi:10.1152/japplphysiol.00954.2005

Dopaminergic regulation of cerebral cortical microcirculation

Nature Neuroscience 1, 286 - 289 (1998)
doi:10.1038/1099
Leonid S. Krimer1, E. Christopher Muly III2, Graham V. Williams1 & Patricia S. Goldman-Rakic1

1 Section of Neurobiology, Yale University School of Medicine, New Haven, Connecticut 06510, USA

2 Department of Psychiatry, Yale University School of Medicine, New Haven, Connecticut 06510, USU

Functional variations in cerebral cortical activity are accompanied by local changes in blood flow, but the mechanisms underlying this physiological coupling are not well understood. Here we report that dopamine, a neurotransmitter normally associated with neuromodulatory actions, may directly affect local cortical blood flow. Using light and electron-microscopic immunocytochemistry, we show that dopaminergic axons innervate the intraparenchymal microvessels. We also provide evidence in an in vitro slice preparation that dopamine produces vasomotor responses in the cortical vasculature. These anatomical and physiological observations reveal a previously unknown source of regulation of the microvasculature by dopamine. The findings may be relevant to the mechanisms underlying changes in blood flow observed in circulatory and neuropsychiatric disorders.

Disturbance of sympathetic cardiovascular regulation is involved in CFS

Wyller VB, Saul JP, Walloe L, Thaulow E "...our results suggest that CFS patients suffer from a more comprehensive disturbance of sympathetic cardiovascular regulation than previously acknowledged, supporting the hypothesis that dysautonomia may be a central etiologic component of CFS (Freeman and Komaroff 1997). Specifically, the sympathetic nervous system is more activated at rest, and seems to have an enhanced response to orthostatic stress, but has a reduced response to the addition of isometric exercise. These abnormalities may account for the high prevalence of orthostatic symptoms among CFS patients.

recent reports have linked cerebral hypoperfusion to abnormalities in cholinergic metabolism

Dr Faisel Khan, Vascular Diseases Research Unit,
University Department of Medicine, Ninewells
Hospital and Medical School, Dundee DD1 9SY, UK

accepted 30 April 2003

Although the aetiology of chronic fatigue syndrome (CFS) is unknown, there have
been a number of reports of blood flow abnormalities within the cerebral circulation
and systemic blood pressure defects manifesting as orthostatic intolerance. Neither
of these phenomena has been explained adequately, but recent reports have linked
cerebral hypoperfusion to abnormalities in cholinergic metabolism. Our group has
previously reported enhanced skin vasodilatation in response to cumulative doses of
transdermally applied acetylcholine (ACh), implying an alteration of peripheral
cholinergic function. To investigate this further, we studied the time course of ACh-
induced vasodilatation following a single dose of ACh in 30 patients with CFS and
30 age- and gender-matched healthy control subjects. No differences in peak blood
flow was seen between patients and controls, but the time taken for the ACh
response to recover to baseline was significantly longer in the CFS patients than in
control subjects. The time taken to decay to 75% of the peak response in patients and
controls was 13Æ7 ± 11Æ3 versus 8Æ9 ± 3Æ7 min (P
1⁄4 0Æ03), respectively, and time
taken to decay to 50% of the peak response was 24Æ5 ± 18Æ8 versus 15Æ1 ± 8Æ9 min
(P
1⁄4 0Æ03), respectively. Prolongation of ACh-induced vasodilatation is suggestive
of a disturbance to cholinergic pathways, perhaps within the vascular endothelium
of patients with CFS, and might be related to some of the unusual vascular
symptoms, such as hypotension and orthostatic intolerance, which are characteristic
of the condition.

Regional temperature rises within the CNS can lead to alteration of membrane properties.

Regional temperature rises within the
CNS can lead to an alteration of mem-
brane properties. For example, enzyme
activity – ornithine decarboxylase – is in-
creased when calcium flows into the cell
via a temperature-sensitive mechanism.
Interestingly, one study observed an acti-
vation of this enzyme after EMF exposure,
subsequently resulting in a temporary per-
meability increase of the BBB.

On the other hand, also a tempo-
rary blood pressure rise could cause an
increase of BBB permeability.

Privatdozent Dr. med. Florian Stögbauer,
University of Münster

Hyperpigmentation after sympathectomy

Hyperpigmentation after sympathectomy

  • 1Departments of Dermatology, Royal Infirmary, Bristol BS2 8HW *Departments of Surgery, Royal Infirmary, Bristol BS2 8HW
  • Clinical and Experimental Dermatology

    Volume 5 Issue 3 Page 349-350, September 1980

Avoidance learning

Chemical sympathectomy and two-way escape and avoidance learning in the rat.

Six experiments are reported on the effects of 2,4,5-trihydroxyphenylethyl-amine (6-hydroxydopamine) on two-way escape and avoidance learning. Rats were tested on either escape or avoidance learning at 80 days of age after chemical sympathectomy at birth or 40 or 80 days of age. Neonatal and chronic sympathectomy (at 40 days), but not acute sympathectomy (at 80 days), resulted in depressed escape learning. Avoidance learning was affected by neonatal sympathectomy and partially by acute sympathectomy. The results have implications for the role of the autonomic nervous system in escape-avoidance learning.
Lord BJ, King MG, Pfister HP
J Comp Physiol Psychol 1976; 90:303-16.

alteration of carbohydrate and lipid metabolism following sympathectomy

Recent Adv Stud Cardiac Struct Metab 1976; 9:259-67.
Imbach A

These results indicate an important alteration of carbohydrate and lipid metabolism after chemical sympathectomy, thus supporting a role of the sympathetic nervous system in their regulation.

sympathectomy on insulin receptors and insulin action

Insulin receptors and effects of insulin on lipolysis, lipogenesis and glucose transport were investigated in fat cells obtained from rats chemically sympathectomized with 6-hydroxydopamine. Four days after a single injection of 6-hydroxydopamine (50 mg/kg), the norepinephrine content of the epididymal adipose tissue was reduced by 97.5%. The number of high-affinity insulin binding sites was increased moderately (16%). In parallel, the sensitivity to insulin of the isoprenaline-stimulated lipolysis was increased as judged from insulin concentrations yielding half-maximal inhibition which were lower (40%) in the treated group. Glucose metabolism, however, was inhibited by chemical sympathectomy: the glucose transport rate was significantly reduced and fatty acid synthesis was nearly totally abolished. Insulin was still effective in stimulating both parameters but failed to restore normal levels. The results suggest that the sympathetic innervation of adipose tissue may exert an inhibitory effect on the number of high-affinity insulin receptors as well as on the sensitivity of the lipolysis to insulin, as both parameters were increased by sympathectomy. To explain the inhibitory effect of 6-hydroxydopamine treatment on glucose transport and fatty acid synthesis, a possible trophic effect of the sympathetic innervation is discussed as well as indirect mechanism counteracting the effects of the chemical sympathectomy.

Effects of chemical sympathectomy on insulin receptors and insulin action in isolated rat adipocytes.



Joost HG, Quentin SH
J Pharmacol Exp Ther 1984; 229:839-44.

relevant to the pathogenesis of human dysautonomias.


Systemic injection of monoclonal antibodies to neural acetylcholinesterase in adult rats caused a syndrome with permanent, complement-mediated destruction of presynaptic fibers in sympathetic ganglia and adrenal medulla. Ptosis, hypotension, bradycardia, and postural syncope ensued. In sympathetic ganglia, acetylcholinesterase activity disappeared from neuropil but not from nerve cell bodies. Choline acetyltransferase activity and ultrastructurally defined synapses were also lost. Electrical stimulation of presynaptic fibers to the superior cervical ganglion ceased to evoke end-organ responses. On the other hand, direct ganglionic stimulation remained effective, and the postganglionic adrenergic system appeared intact. Motor performance and the choline acetyltransferase content of skeletal muscle were preserved, as was parasympathetic (vagal) function. This model of selective cholinergic autoimmunity represents another tool for autonomic physiology and may be relevant to the pathogenesis of human dysautonomias.

Norepinephrine depletion commonly is the desired effect, other neurotransmitters (eg ATP, NPY and enkephalins) are depleted by sympathectomy

The term Sympathectomy used in this discussion refers mainly to the lesioning of postganglionic noradrenergic (NA) neurons and fibers except where noted. Although norepinephrine depletion commonly is the desired effect, other costored neurotransmitters (eg ATP, NPY and enkephalins) are depleted by sympathetic denervation. The multitude of research studying the effects of sympathetic loss is made possible by the morphologically defined anatomy of the postganglionic sympathetic chains, the sensitivity of postganglionic NA neurons to nerve growth factor (NGF) deprivation, and the phenotypic specialty of these neurons that allows for the selective uptake of neurotoxins.

Primer on the Autonomic Nervous System

By David Robertson
Published 2004

Serum Dopamine-β -Hydroxylase: Decrease after Chemical Sympathectomy

Dopamine-β -hydroxylase is an enzyme that is localized to catecholamine-containing vesicles in sympathetic nerves and the adrenal medulla, and is also found in the serum. Treatment of rats with 6-hydroxydopamine, a drug which destroys sympathetic nerve terminals, leads to a decrease in serum dopamine-β -hydroxylase activity.



Weinshilboum, Richard; Axelrod, Julius
Publication:
Science, Volume 173, Issue 4000, pp. 931-934
Publication Date:
09/1971
Origin:
JSTOR

In the adrenal medulla, AChE-rich presynaptic fibers disappeared within 3 days


  • In the adrenal medulla, AChE-rich presynaptic fibers disappeared within 3 days
  • Autoimmune Preganglionic Sympathectomy Induced by Acetylcholinesterase Antibodies
  • Stephen Brimijoin and Vanda A. Lennon
  • Proceedings of the National Academy of Sciences of the United States of America, Vol. 87, No. 24 (Dec., 1990), pp. 9630-9634 (article consists of 5 pages)
  • Published by: National Academy of Sciences

intact adrenal medulla was essential for SHR groups to achieve many of the adaptations associated with training.

Responses of SHR to combinations of chemical sympathectomy, adrenal demedullation, and training

C. M. Tipton, M. S. Sturek, R. A. Oppliger, R. D. Matthes, J. M. Overton and J. G. Edwards

The single and combined influences of exercise training, chemical sympathectomy (SYMX), and surgical adrenal demedullation (D) were examined in four separate spontaneously hypertensive rat (SHR) groups. SYMX was accomplished by subcutaneous injections of antinerve growth factor (ANGF) over a 5-day period after birth followed by 20 separate injections of guanethidine sulfate during a 27-day period. Measurements of urine, plasma, or tissue levels of catecholamines indicated that these experimental procedures were effective. The animals were exercise trained (T) for 10 wk or longer at 40-60% of their VO2max capacity, and all T groups exhibited longer run times or higher muscle cytochrome oxidase activity; however, only the SHR + T subgroup had a significantly higher VO2max value than its control (NT). Training lowered resting systolic blood pressure (SBP) in the SHR subgroup but normalization of SBP occurred only with SYMX. Interestingly, only the SYMX + T subgroup with intact adrenal glands also had lower SBP values than the NT. The SHR + T and SYMX + T subgroups but not the SYMX + D + T had less cardiac acceleration after ip injections of atropine than their controls. Heavier heart weights were observed only in the SHR + T subgroup; SYMX was associated with lighter heart weights regardless of whether the rats had been T or D. These collective findings demonstrated again the importance of the sympathetic nervous system to an exercise response, suggesting that an intact adrenal medulla was essential for SHR groups to achieve many of the adaptations associated with training.
Am J Physiol Heart Circ Physiol 247: H109-H118, 1984;
0363-6135/84 $5.00

no one has examined the effects of sympathectomy, adrenergic blockade, or adrenal demedulation

Thus, until proven otherwise, we suggest that many, if not all, of the anti-inflammatory effects associated with efferent vagal stimulation are due to the concurrent activation of the adrenal medulla and the sympathetic nervous system. It is surprising that no one has examined the effects of sympathectomy, adrenergic blockade, or adrenal demedulation on the inhibition of TNF-� and inflammation produced by efferent vagal stimulation.

PubMed articles by:
Autonomic Innervation and Regulation of the Immune System
(1987-2007)
Dwight M. Nance and Virginia M. Sanders
Brain Behav Immun. 2007 August; 21(6): 736–745.


Madden KS, Felten SY, Felten DL, Sundaresan PR, Livnat S.
Sympathetic neural modulation of the immune system. I.
Depression of T cell immunity in vivo and in vitro following chemical sympathectomy. Brain Behav.Immun.
1989;3:72–89. [PubMed]


HYPOTHALAMUS:

RECENT STUDIES ON THE HYPOTHALAMUS:
K. E. COOPER
TEMPERATURE REGULATION AND THE HYPOTHALAMUS
Br. Med. Bull., September 1966; 22: 238 - 242.
*......pathway is necessary for the complete febrile response in cats was shown by Knkston (1935), who found that complete bilateral sympathectomy greatly reduced the pyrogenic response, and by Douglas (1954), who showed the importance of ear vasoconstriction in the......