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

Thursday, December 18, 2008

complex alterations of vascular reactivity

Enhanced vascular reactivity in the sympathectomized rat: studies in vivo and in small isolated resistance arteries.

Conclusions: In conclusion, we showed that sympathectomy produces complex alterations of vascular reactivity both in vivo and in isolated vessels, which shift the balance of the sensitivity of the vessel between vasoconstrictor and vasodilating agents towards an increased constriction. These results are unlikely to simply reflect denervation supersensitivity; their underlying receptor, post-receptor and/or contractile mechanisms are yet to be identified.

Journal of Hypertension. 18(8):1041-1049, August 2000.
Rizzoni, Damiano 1; Perlini, Stefano 2,3; Mircoli, Luca 2; Porteri, Enzo 1; Franzelli, Cristina 2; Castellano, Maurizio 1; Rosei, Enrico Agabiti 1; Ferrari, Alberto U. 2,4

Abnormal pain following nerve sprouting

Collectively, our findings indicate that as a result of autonomic sprouting due to CCI of the MN, remaining intact nociceptive fibres may potentially develop sensitivity to sympathetic and parasympathetic stimulation, which may have a role in the generation of abnormal pain following nerve injury.

Received 22 October 2004, revised 17 February 2005, accepted 23 February 2005

C. Grelik 1 , G. J. Bennett 3,4,5 and A. Ribeiro-da-Silva 1,2,5
1 Department of Pharmacology & Therapeutics, McGill University, 3655 Prom. Sir-William-Osler, Montreal, Quebec, Canada H3G 1Y6
2 Department of Anatomy and Cell Biology,
3 Department of Anesthesia,
4 Faculty of Dentistry, and
5 McGill Centre for Research on Pain, McGill University, Montreal, Quebec, Canada

Summary from the University of Cambridge

ANDBN, MAGNUSSON and ROSENGREN (1965)
have demonstrated a complete loss of DOPA decarboxylase activity of iris, spleen
and submaxillary gland after surgical sympathectomy, and a complete loss of tyrosine
hydroxylase activity of heart, submaxillary gland and kidney has been found after
surgical sympathectomy (POOL, COVELL, LEVITT, GIBB and BRAUNWALD, 1967;
SEDVALL and KOPIN, 1967; NAGATSU, RUST and DE QUATTRO, 1969). Although the
time course of the fall in DOPA decarboxylase and tyrosine hydroxylase activities
of operated vasa was not investigated, a preliminary experiment showed that all
DOPA decarboxylase activity was absent one day after denervation. Thus, it seems
likely that these two enzymes which are involved in the biosynthesis of NA have
a cellular localization within the sympathetic nerves of the vas deferens.
NORADRENALINE METABOLIZING ENZYMES IN
NORMAL AND SYMPATHETICALLY DENERVATED
VAS DEFERENS
B. JARROTTI and L. L. IVERSEN
Department of Pharmacology, University of Cambridge, Cambridge, England
(Received 5 May 1970. Accepted 21 May 1970)

Sympathectomy causes diminished capacity for physical sensation

Results: In the hot-plate analgesia test, sympathectomized rats increased their hot-plate latency time compared with that of sham-operated rats. Density of calcitonin gene-related peptide immunoreactive fibers in sympathectomy side of the lumbar dura mater decreased to 45.5% compared with the contralateral side. The number and size of calcitonin gene-related peptide immunoreactive cells in dorsal root ganglia showed no difference between sympathectomized and contralateral side.

Conclusion: Sympathectomy increased the pain threshold and made the sympathectomized rats hypesthetic.

An Anatomic Study of Neuropeptide Immunoreactivities in the Lumbar Dura Mater After Lumbar Sympathectomy.

Spine. 21(8):925-930, April 15, 1996.
Sekiguchi, Yasufumi MD *+; Konnai, Yasunobu MD *+; Kikuchi, Shinichi MD, PhD *; Sugiura, Yasuo MD, PhD +

Long-term superior cervical sympathectomy induces mast cell hyperplasia and increases histamine and serotonin content

Nerve fibres and mast cells are often described in close morphological and functional interactions in various organs such as the dura mater. The respective roles of mast cell activation and sympathetic impairment in cluster headache and migraine attacks have been repeatedly suggested. We have thus investigated the long-term effects of sympathectomy on mast cell morphology and content in the rat dura mater.
After unilateral ganglionectomy, the histamine content increased progressively and significantly 30–60 days post-surgery in both hemi-dura, whereas the serotonin content became significantly different from that of sham only 60 days post-surgery in the ipsilateral dura. After bilateral ganglionectomy, the histamine level significantly increased in both hemi-dura 15–60 days post-surgery, whereas the serotonin level had significantly increased at 60 days post-surgery.

These results clearly demonstrate, for the first time, a long-term trophic effect of sympathetic nerve degeneration on mast cells in the dura mater.

A. Bergerot*, A. -M. Reynier-Rebuffel, J. Callebert and P. Aubineau

Copyright © 1999 IBRO. Published by Elsevier Science Ltd.

Mast cell hyperplasia: role of cytokines.


Department of Gastroenterology, Hepatology and Endocrinology, Medical School of Hannover, Germany

Mast cell hyperplasia is found in different pathologies such as chronic inflammatory processes, fibrotic disorders, wound healing or neoplastic tissue transformation. The functional significance of the accumulation of mast cells in these processes is largely unknown. It is now established that bone marrow-derived mast cell progenitors circulate in peripheral blood and subsequently migrate into the tissue where they undergo final maturation under the influence of local microenvironmental factors. Cytokines are of particular importance for mast cell recruitment, development, and function. Stem cell factor (SCF) is a unique mast cell growth factor, since mast cells disappear completely in the absence of SCF. However, several other cytokines such as IL-3 and IL-4 have been shown to influence mast cell proliferation and function also. This review focuses on the role of cytokines in the regulation of mast cell hyperplasia. Copyright 2002 S. Karger AG, Basel

Int Arch Allergy Immunol. 2002 Feb;127(2):118-22.Click here to read

Sympathectomy increases chronic DSS colitis

Sympathectomy reduced acute DSS colitis but increased chronic DSS colitis. Sympathectomy also increased chronic colitis in Il10–/– mice.

Anti-inflammatory role of sympathetic nerves in chronic intestinal inflammation

R H Straub1, F Grum1, U Strauch1, S Capellino1, F Bataille2, A Bleich3, W Falk1, J Schölmerich1, F Obermeier1

1 Laboratory of Neuroendocrino-Immunology, Department of Internal Medicine I, University Hospital Regensburg, Germany
2 Department of Pathology, University of Regensburg, Regensburg, Germany
3 Institute for Laboratory Animal Science and Central Animal Facility, Hannover Medical School, Hannover, Germany

Published Online First: 28 February 2008. doi:10.1136/gut.2007.125401
Gut 2008;57:911-921
Copyright © 2008 BMJ Publishing Group Ltd & British Society of Gastroenterology

destroying the sympathetic nerves and their ability to transmit impulses

Surgery (Endoscopic thoracic sympathectomy or ETS): Select sympathetic nerves or nerve ganglia in the chest are either cut or burned (completely destroying their ability to transmit impulses), or clamped (theoretically allowing for the reversal of the procedure). The procedure often causes anhidrosis from the mid-chest upwards, a disturbing condition. Major drawbacks to the procedure include thermo regulatory dysfunction (Goldstein, 2005), lowered fear and alertness and the overwhelming incidence of compensatory Hyperhydrosis. Some people find this sweating to be tolerable while others find the compensatory Hyperhydrosis to be worse than the initial condition. It has also been established that there is a low (less than 1%) chance of Horner's syndrome. Other risks common to minimally-invasive chest surgery, though rare, do exist. Patients have also been shown to experience a cardiac sympathetic denervation, which results in a 10% lowered heartbeat during both rest and exercise. ETS was thought to be helpful in treating facial blushing and facial sweating. According to Dr. Reisfeld,the only indication for ETS at present is excessive and severe palmar Hyperhydrosis (excessive hand sweating). Statistics have shown that when treated for facial blushing and/or excessive facial sweating, the failure rate of ETS for those two clinical presentations is higher and patients are more prone to side effects.
http://immersivemedical.com/hyperhydrosis_fr_2.html

Changes in Electrophysiology following sympathectomy

Chemical sympathectomy was obtained following intravenous injection of 50 mg·kg–1 of 6-hydroxydopamine. Sympathectomised dogs presented significant increases in: basic sinus period, sino-atrial conduction time (SACT), AH and HV intervals of the His bundle electrogram, atrial functional (AFRP) and effective (AERP) refractory periods, atrio-ventricular node functional (AVNFRP) and effective (AVNERP) refractory periods, ventricular functional (VFRP) and effective (EVRP) refractory periods and atrial (AMAP) and ventricular (VMAP) monophasic action potential durations. Corrected sinus recovery time (CSRT) was not affected by chemical sympathectomy. Neither was the atrial ERP/MAP duration ratio. This new form of sympathectomy affects all the levels of the cardiac conduction system. Such results are in accordance with those obtained with surgical sympathectomy or the use of beta-blocking agents.

DIANE GODIN*, CLAUDE GUIMOND{dagger}, RÉGINALD A NADEAU{ddagger} and A ROBERT LEBLANC§

From the Department of Physiology, Faculty of Medicine, Université de Montréal and Centre de recherche, Hôpital du Sacré-Coeur, Montréal, Canada

Cardiovascular Research 1982 16(9):524-529; doi:10.1093/cvr/16.9.524
© 1982 by European Society of Cardiology

Sympathectomy frequently causes perioperative hypotension

Vasomotor output is modified by inputs from throughout the central nervous system, including the hypothalamus, cerebral cortex, and the other areas in the brain stem. Areas in the posterolateral medulla receive input from both the vagal and the glossopharyngeal nerves and play an important role in mediating a variety of circulatory reflexes. The sympathetic system normally maintains some tonic vasoconstriction on the vascular tree. Loss of this tone following induction of anesthesia or sympathectomy frequently contributes to perioperative hypotension.

Clinical Anesthesiology
By G. Edward Morgan, Maged S. Mikhail, Michael J. Murray
Published by McGraw-Hill Professional, 2005
ISBN 0071423583, 9780071423588

hypoxic response after sympathectomy

Blockade of the sympathetic nervous system with {alpha} ... (9) reported a reduction in the hypoxic response of the lung after sympathectomy. ...
www.anesthesia-analgesia.org/cgi/content/full/88/3/494

by I Garutti - 1999

autoregulatory breakthrough is eliminated when the arterial baroreflex is interrupted

The effects of sympathetic section blockade are greater during systemic hypercapnia than during normocapnia: a decrease in cerebrovascular resistance has been demonstrated in cats and rabbits after bilateral sympathectomy when PaCO2 was below 62-67 mmHg.
Blockade of sympathetic activity causes a significant further increase in CBF during hypoxia.

..sympathetic activation exerts a significant protective action on CBF and blood-brain barrier (BBB) permeability (Bill and Lander 1976) an effect which is also seen in the presence of moderate increase increases in BP, where autoregulation maintains CBF almost constant.

The vasodilation which characterizes autoregulatory breakthrough is eliminated when the arterial baroreflex is interrupted (Talman et al. 1994), which suggests that it is an active process. It is possible that the breakthrough depends on release of nitric oxide or a NO donor associated with the removal of the sympathetic innervation of cerebral vessels (Talman and Dragon 1995).

Intoxications of the Nervous System
By Pierre J. Vinken, F. A. de Wolff, George W. Bruyn, Otto Appenzeller, Harold L. Klawans
Published by Elsevier Health Sciences, 1999
ISBN 0444828133, 9780444828132

Effects of Sympathetic Nervous System activation

Our previous work indicates that myocardial ischemia could be the mechanism responsible for the left ventricular (LV) dysfunction that frequently develops after massive sympathetic nervous system (SNS) activation. In this study, coronary blood flow (CBF) and myocardial ATP, creatine phosphate, and lactate concentrations were measured after massively activating the SNS of anesthetized rabbits with an intracisternal injection of veratrine. CBF was measured at time 0 (baseline), and at 2, 10, and 20 min after SNS activation in one group, and at 0, 45, 90, and 150 min in a second group. Myocardial ATP, creatine phosphate, and lactate were measured at 0, 2, 10, 20, 90, and 150 min in separate groups of rabbits. SNS activation caused LV dysfunction in ~60% of the rabbits. SNS-related increases in CBF kept pace with the increases in myocardial energy demand as determined from the systolic pressure-heart rate product. The subendocardial-to-subepicardial blood flow ratio did not change significantly. Myocardial creatine phosphate concentration was depressed 2 min after SNS activation and remained depressed for at least 20 min. ATP fell continuously and was significantly lower than baseline by 20 min. Tissue lactate concentration was elevated at this time.
Jennifer M. Smith and Charles F. Pilati,1

Department of Physiology, Northeastern Ohio University College of Medicine, Rootstown, Ohio 44272

Experimental Biology and Medicine 227:125-132 (2002)
© 2002 Society for Experimental Biology and Medicine