'Sympathetic ablation alters lymphocyte membrane properties'

K Miles, E Chelmicka-Schorr, S Atweh, G Otten, and BG Arnason
J. Immunol., Aug 1985; 135: 797 - 801. 

Our results show that [3H]substance P binding in the intermediolateral cell column is dependent on the integrity of sympathetic postganglionic neurons

Guanethidine-induced destruction of sympathetic postganglionic neurons in neonatal rats leads to transneuronal degeneration of the sympathetic preganglionic neurons. Using this model, we have been able to show a approximately 35% decrease in [3H]substance P ([3H]SP) binding in the intermediolateral cell column--suggesting that sympathetic preganglionic neurons possess substance P receptors. Our results show that [3H]substance P binding in the intermediolateral cell column is dependent on the integrity of sympathetic postganglionic neurons.

Brain Res. 1985 Apr 29;193-6. pii:0006-8993(85)90146-5.
Reduction of [3H]substance P binding in the intermediolateral cell column after sympathectomy. Takano Y,Loewy AD
https://www.gcbi.com.cn/gclib/html/pubmed/detail/2581658

https://archive.is/bfPLv

Substance P is an important element in pain perception. The sensory function of substance P is thought to be related to the transmission of pain information into the central nervous system. Substance P coexists with the excitatory neurotransmitter glutamate in primary afferents that respond to painful stimulation.[16] Substance P has been associated with the regulation of mood disorders, anxiety, stress,[17] reinforcement,[18] neurogenesis,[19] respiratory rhythm,[20] neurotoxicity, nausea and emesis,[21] pain, and nociception.[22] Substance P and other sensory neuropeptides can be released from the peripheral terminals of sensory nerve fibers in the skin, muscle, and joints. It is proposed that this release is involved in neurogenic inflammation, which is a local inflammatory response to certain types of infection or injury.[23] The regulatory function of SP also involves the regulation of its high-affinity receptor, NK-1. Substance P receptor antagonists may have important therapeutic applications in the treatment of a variety of stress-related illnesses, in addition to their potential as analgesics.

https://en.wikipedia.org/wiki/Substance_P

sympathectomy-induced immune alterations

Brain Behav Immun. 2002 Feb;16(1):33-45.

The effects of chemical sympathectomy on T-cell cytokine responses are not mediated by altered peritoneal exudate cell function or an inflammatory response.

Callahan TA1, Moynihan JA.

Author information

Abstract

Ablation of the sympathetic nervous system by chemical sympathectomy is a standard model for the study of sympathetic nervous system regulation of immune function. We have previously documented that chemical denervation results in enhanced antigen-specific, but suppressed mitogen-induced, cytokine production by spleen cells. In our investigation into the mechanisms of sympathectomy-induced immune alterations, we first evaluated the peritoneal environment into which the protein antigen keyhole limpet hemocyanin is administered. Denervation resulted in increased production of tumor necrosis factor-alpha by peritoneal exudate cells and these cells appeared to have enhanced antigen presenting capability. We hypothesized that nerve terminal destruction may be inducing an inflammatory response by monocyte/macrophages and other cell types throughout the periphery that could differentially alter subsequent mitogen versus antigen-specific responses. However, no evidence of sympathectomy-induced systemic or local splenic inflammatory responses was observed, as indicated by measuring the proinflammatory cytokines tumor necrosis factor-alpha and interleukin-1beta. These experiments indicate that an inflammatory response is not likely to be responsible for sympathectomy-induced immune alterations, eliminating a potential confounding factor in interpreting sympathectomy studies.

Copyright 2001 Elsevier Science (USA).

the clinical results of both surgical and neurolityc sympathectomy are uncertain

Blood diverted from muscle to skin after sympathectomy

However, the clinical results of both surgical and neurolityc sympathectomy are uncertain. Indeed these procedures lead to a redistribution of the blood flow in the lower limbs from the muscle to the skin, with a concomitant fall of the regional resistance, mainly in undamaged vessels. The blood flow will be diverted into this part of the vascular tree, so that a "stealing" of the blood flow may occur.

Vito A. Peduto, Giancarlo Boero, Antonio Marchi, Riccardo Tani

Bilateral extensive skin necrosis of the lower limbs following prolonged epidural blockade

Anaesthesia 1976; 31: 1068-75.

Surgical and chemical sympathectomy can alter cellular proliferation

Surgical denervation and chemical sympathectomy can alter cellular proliferation, B- and T-cell responsiveness and lymphocyte migration in lymphoid organs [17]. In vitro studies have shown that neuropeptides can have numerous effects, either inhibiting or stimulating the proliferation, differentiation and functions of immune cells [19]*

Development of systemic lupus erythematosus in mice is associated with alteration of neuropeptide concentrations in inflamed kidneys and immunoregulatory organs
Neuroscience Letters 248 (1998) 97– 100

Ablation of the sympathetic nervous system is a standard model for the study of sympathetic nervous system regulation of immune function

Ablation of the sympathetic nervous system by chemical sympathectomy is a standard model for the study of sympathetic nervous system regulation of immune function. We have previously documented that chemical denervation results in enhanced antigen-specific, but suppressed mitogen-induced, cytokine production by spleen cells. In our investigation into the mechanisms of sympathectomy-induced immune alterations, we first evaluated the peritoneal environment into which the protein antigen keyhole limpet hemocyanin is administered. Denervation resulted in increased production of tumor necrosis factor- by peritoneal exudate cells and these cells appeared to have enhanced antigen presenting capability. We hypothesized that nerve terminal destruction may be inducing an inflammatory response by monocyte/macrophages and other cell types throughout the periphery that could differentially alter subsequent mitogen versus antigen-specific responses. However, no evidence of sympathectomy-induced systemic or local splenic inflammatory responses was observed, as indicated by measuring the proinflammatory cytokines tumor necrosis factor- and interleukin-1. These experiments indicate that an inflammatory response is not likely to be responsible for sympathectomy-induced immune alterations, eliminating a potential confounding factor in interpreting sympathectomy studies. Copyright 2001 Elsevier Science (USA).

Authors: Callahan T.A.^{1, 2}; Moynihan J.A.^{1, 2, 3, 4, 5}
Source: Brain, Behavior, and Immunity, Volume 16, Number 1, February 2002 , pp. 33-45(13)

Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome

Pain. 1996 Jan;64(1):1-9.

Post-sympathectomy neuralgia: hypotheses on peripheral and central neuronal mechanisms.

Kramis RC1, Roberts WJ, Gillette RG.

Author information

Abstract

Post-sympathectomy neuralgia is proposed here to be a complex neuropathic and central deafferentation/reafferentation syndrome dependent on: (a) the transection, during sympathectomy, of paraspinal somatic and visceral afferent axons within the sympathetic trunk; (b) the subsequent cell death of many of the axotomized afferent neurons, resulting in central deafferentation; and (c) the persistent sensitization of spinal nociceptive neurons by painful conditions present prior to sympathectomy. Viscerosomatic convergence, collateral sprouting of afferents, and mechanisms associated with sympathetically maintained pain are all proposed to be important to the development of the syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/8867242

Mast cells and nerve growth factor (NGF) have both been reported to be involved in neuroimmune interactions and tissue inflammation

Proc Natl Acad Sci U S A. 1994 Apr 26;91(9):3739-43.

Mast cells synthesize, store, and release nerve growth factor.

Leon A1, Buriani A, Dal Toso R, Fabris M, Romanello S, Aloe L, Levi-Montalcini R.

Author information

Abstract

Mast cells and nerve growth factor (NGF) have both been reported to be involved in neuroimmune interactions and tissue inflammation. In many peripheral tissues, mast cells interact with the innervating fibers. Changes in the behaviors of both of these elements occur after tissue injury/inflammation. As such conditions are typically associated with rapid mast cell activation and NGF accumulation in inflammatory exudates, we hypothesized that mast cells may be capable of producing NGF. Here we report that (i) NGF mRNA is expressed in adult rat peritoneal mast cells; (ii) anti-NGF antibodies clearly stain vesicular compartments of purified mast cells and mast cells in histological sections of adult rodent mesenchymal tissues; and (iii) medium conditioned by peritoneal mast cells contains biologically active NGF. Mast cells thus represent a newly recognized source of NGF. The known actions of NGF on peripheral nerve fibers and immune cells suggest that mast cell-derived NGF may control adaptive/reactive responses of the nervous and immune systems toward noxious tissue perturbations. Conversely, alterations in normal mast cell behaviors may provoke maladaptive neuroimmune tissue responses whose consequences could have profound implications in inflammatory disease states, including those of an autoimmune nature.

http://www.ncbi.nlm.nih.gov/pubmed/8170980

Lung India. 2015 Jan-Feb;32(1):73-5. doi: 10.4103/0970-2113.148458.

Thoracic sympathectomy for peripheral vascular disease can lead to severe bronchospasm and excessive bronchial secretions.

Goyal VD1, Gupta B2, Kumar S3, Pal S4.

A 57-year-old male patient suffering from Buerger's disease presented with pre-gangrenous changes in right foot and ischemic symptoms in right hand. Computed tomographic angiography revealed diffuse distal disease not suitable for vascular bypass and angioplasty. Right lumbarsympathectomy was done using a retroperitoneal approach followed 1 year later by right thoracic sympathectomy using a transaxillary approach. Postoperatively, the patient had severe bronchospasm and excessive secretions in the respiratory tract resistant to theophylline and sympathomimetic group of drugs and without any clinical, laboratory and radiological evidence of infection. The patient was started on anticholinergics in anticipation that sympathectomy might have lead to unopposed cholinergic activity and the symptoms improved rapidly. The patient recovered well and was discharged on 10(th) post-operative day.

http://www.ncbi.nlm.nih.gov/pubmed/25624604

cervical sympathectomy induced mast cell hyperplasia and increased histamine and serotonin content in the dura mater

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

Long-term superior cervical sympathectomy induces mast cell hyperplasia and increases histamine and serotonin content in the rat dura mater, 

Neuroscience 96 (2000) 205–213. 


Mast cells are critical players in allergic reactions, but they have also been shown to be important in immunity and recently also in inflammatory diseases, especially asthma. Migraines are episodic, typically unilateral, throbbing headaches that occur more frequently in patients with allergy and asthma implying involvement of meningeal and/or brain mast cells. These mast cells are located perivascularly, in close association with neurons especially in the dura, where they can be activated following trigeminal nerve, as well as cervical or sphenopalatine ganglion stimulation. Neuropeptides such as calcitonin gene-related peptide (CGRP), hemokinin A, neurotensin (NT), pituitary adenylate cyclase activating peptide (PACAP), and substance P (SP) activate mast cells leading to secretion of vasoactive, proinflammatory, and neurosensitizing mediators, thereby contributing to migraine pathogenesis. Brain mast cells can also secrete proinflammatory and vasodilatory molecules such as interleukin-6 (IL-6) and vascular endothelial growth factor (VEGF), selectively in response
to corticotropin-releasing hormone (CRH), a mediator of stress which is known to precipitate or exacerbate migraines. A better understanding of brain mast cell activation in migraines would be useful and could lead to several points of prophylactic intervention.

D 2005 Elsevier B.V. All rights reserved.

Brain Research Reviews 49 (2005) 65 – 76
The role of mast cells in migraine pathophysiology
Theoharis C. Theoharides*, Jill Donelan,
Kristiana Kandere-Grzybowska1

, Aphrodite Konstantinidou2

chronic interference with β-adrenergic receptors (via either sympathectomy or β-blockade) on cardiac mast cell morphology/activation and on interstitial collagen deposition

In the present study we investigated the effects of chronic interference with β-adrenergic receptors (via either sympathectomy or β-blockade) on cardiac mast cell morphology/activation and on interstitial collagen deposition. In rats subjected to chemical sympathectomizy with the neuro- toxin 6-hydroxydopamine (6-OHDA) we observed a significant increase of mast cell density, and in particular of degranulat- ing mast cells, suggesting a close relationship between the cardiac catecholaminergic system and mast cell activation. In parallel, chronic 6-OHDA treatment was associated with increased collagen deposition. The influence of the β-adren- ergic receptor component was investigated in rats subjected to chronic propranolol administration, that caused a further significant increase in mast cell activation associated with a lower extent of collagen deposition when compared to chem- ical sympathectomy. These data are the first demonstration of a close relationship between rat cardiac mast cell activation and the catecholaminergic system, with a complex interplay with cardiac collagen deposition. Specifically, abrogation of the cardiac sympathetic efferent drive by chemical sympathectomy causes mast cell activation and interstitial fibrosis, possibly due to the local effects of the neurotoxin 6-hydroxy- dopamine. In contrast, β-adrenergic blockade is associated with enhanced mast cell degranulation and a lower extent of collagen deposition in the normal myocardium. In conclusion, cardiac mast cell activation is influenced by β-adrenergic influences. 

http://www.ejh.it/index.php/ejh/article/viewFile/985/1108

Correspondence: Rosanna Nano,
Department of Animal Biology, University of Pavia,

European Journal of Histochemistry

2006; vol. 50 issue 2 (Apr-Jun):133-140

sympathetic denervation disturbed the patterns of gut immune-associated cell distribution

These findings indicated that sympathetic denervation disturbed the patterns of gut immune-associated cell distribution. It would substantiate the thesis of neuro-immune-endocrine and provide the new ideas for the intestinal disease prevention and drug developments.

http://scialert.net/fulltext/?doi=ajava.2011.935.943&org=10

Related articles

• "sympathicotomy may cause a temporary impairment of the caudal-to-rostral hierarchy of thermoregulatory control and changes in microcirculation"
• 2014 Dubious Innovations In Cardiology

direct injury to the anatomic structure of the autonomic nervous system in the thoracic cavity, and postthoracotomy pain may contribute independently or in association with each other to the development of these arrhythmias

Anesthesiol Res Pract. 2013;2013:413985. doi: 10.1155/2013/413985. Epub 2013 Oct 23.

Supraventricular arrhythmias after thoracotomy: is there a role for autonomic imbalance?

Vretzakis G1, Simeoforidou M, Stamoulis K, Bareka M.

Author information

Abstract

Supraventricular arrhythmias are common rhythm disturbances following pulmonary surgery. The overall incidence varies between 3.2% and 30% in the literature, while atrial fibrillation is the most common form. These arrhythmias usually have an uneventful clinical course and revert to normal sinus rhythm, usually before patent's discharge from hospital. Their importance lies in the immediate hemodynamic consequences, the potential for systemic embolization and the consequent long-term need for prophylactic drug administration, and the increased cost of hospitalization. Their incidence is probably related to the magnitude of the performed operative procedure, occurring more frequently after pneumonectomy than after lobectomy. Investigators believe that surgical factors (irritation of the atria per se or on the ground of chronic inflammation of aged atria), direct injury to the anatomic structure of the autonomic nervous system in the thoracic cavity, and postthoracotomy pain may contribute independently or in association with each other to the development of these arrhythmias. This review discusses currently available information about the potential mechanisms and risk factors for these rhythm disturbances. The discussion is in particular focused on the role of postoperative pain and its relation to the autonomic imbalance, in an attempt to avoid or minimize discomfort with proper analgesia utilisation.

http://www.ncbi.nlm.nih.gov/pubmed/24235971

"Since changes in old age show some similarities with those following chronic sympathectomy"

"For the tracheobronchial tree. surgical (sympathectomy) and chemical (with 6-hydroxydopamine or reserpine) interventions lead to histological disappearance of the NA and NPY." (p.435)

" Prejunctional supersensitivity to norepinephrine after sympathectomy or cocaine treatment." (p. 410)

"Following chronic sympathectomy, substance P expression in presumptive sensory nerves....and NPY-expression in parasympathetic nerves ...to autonomically innervated tissues have both been shown to increase... Experiments using NGF and anti-NGF antibodies (Kessler et al., 1983) have suggested that competition between sympathetic and sensory fibers for target-derived growth factors could explain these apparently compensatory interactions,..." (p. 33)

"Since changes in old age show some similarities with those following chronic sympathectomy, it is tempting to consider whether alterations in one group of nerves in tissues with multiple innervations trigger reciprocal changes in other populations of nerves, perhaps through the mechanism of competition for common, target-produced growth factors. The nature of these changes is such that they could be nonadaptive and even destabilizing of cardiovascular homeostasis. (p. 34) 

Impairment of sympathetic and neural function has been claimed in cholesterol-fed animals (Panek et al., 1985). It has also been suggested that surgical sympathectomy may be useful in controlling atherosclerosis in certain arterial beds (Lichter et al., 1987). Defective cholinergic arteriolar vasodilation has been claimed in atherosclerotic rabbits (Yamamoto et al., 1988) and, in our laboratory, we have recently shown impairment of response to perivascular nerves supplying the mesenteric, hepatic, and ear arteries of Watanabe heritable hyperlipidemic rabbits (Burnstock et al., 1991). 
   Loss of adrenergic innervation has been reported in alcoholism (Low et al., 1975), amyloidosis (Rubenstein et al., 1983), orthostatic hypotension (Bannister et al., 1981), and subarachnoid haemorrhage (Hara and Kobayashi, 1988). Recent evidence shows that there is also a loss of noradrenergic innervation of blood vessels supplying malignant, as compared to benign, human intracranial tumours (Crockard et al., 1987). (p. 14)  

Vascular Innervation and Receptor Mechanisms: New    Perspectives 

Rolf Uddman

Academic Press, 2 Dec 2012 - Medical - 498 pages

sympathectomy leads to fluctuation of vasoconstriction alternated with vasodilation in an unstable fashion. Following sympathectomy the involved extremity shows regional hyper - and hypothermia

"To quote Nashold, referring to sympathectomy, "Ill- advised surgery may tend to magnify the entire symptom complex"(38). Sympathectomy is aimed at achieving vasodilation. The neurovascular instability (vacillation and instability of vasoconstrictive function), leads to fluctuation of vasoconstriction alternated with vasodilation in an unstable fashion (39). Following sympathectomy the involved extremity shows regional hyper - and hypothermia in contrast, the blood flow and skin temperature on the non- sympathectomized side are significantly lower after exposure to a cold environment (39). This phenomenon may explain the reason for spread of CRPS. In the first four weeks after sympathectomy, the Laser Doppler flow study shows an increased of blood flow and hyperthermia in the extremity (40). Then, after four weeks, the skin temperature and vascular perfusion slowly decrease and a high amplitude vasomotor constriction develops reversing any beneficial effect of surgery (39). According to Bonica , "about a dozen patients with reflex sympathetic dystrophy (RSD) in whom I have carried out preoperative diagnostic sympathetic block with complete pain relief, sympathectomy produced either partial or no relief (40)"

Chronic Pain: 

 Reflex Sympathetic Dystrophy : Prevention and Management

Hooshang Hooshmand

CRC PressINC, 1993 - Medical - 202 pages

Despite the simplicity and rapidity of the procedure, some patients experience intense, in some cases persistent, postoperative pain

Jornal Brasileiro de Pneumologia - The incidence of residual pneumothorax after video-assisted sympathectomy with and without pleural drainage and its effect on postoperative pain:

"Anteroposterior chest X-ray in the orthostatic position, while inhaling, was absolutely normal in 18 patients (32.1%), and residual pneumothorax was detected in 17 patients (30.4%). When the patients were separated into two groups (those who had received drainage and those who had not), 25.9% (7 patients) and 34.4% (10 patients), respectively, presented residual pneumothorax, with no difference between the two groups (p = 0.48) (Figure 1).

The additional alterations were laminar atelectasis and emphysema of the subcutaneous cellular tissue.

Chest X-rays in the orthostatic position, while exhaling, revealed residual pneumothorax in 39.3% (22 patients) and was absolutely normal in 25% (14 patients). On the same X-rays, when patients were analyzed separately, residual pneumothorax was seen in 33.3% of the patients who had received drainage (9 patients) and in 44.8% (13 patients) of those who had not, with no difference between the two groups (p = 0.37) (Figure 1).

The low-dose computed tomography scans of the chest detected residual pneumothorax in 76.8% (43 patients). In the patients submitted to postoperative drainage, this rate was 70.3% (19 patients), compared with 82.7% (24 patients) in those without pleural drainage, with no difference between the two groups (p = 0.27) (Figure 1). Therefore, the overall rate of occult pneumothorax (only visible through tomography), revealed on anteroposterior X-rays was 35.7% (20 patients): 48.2% while patients were inhaling and 41.1% while patients were exhaling. The VAS score in the PACU ranged from 0 to 10, with a mean of 2.16 ± 0.35.

Regarding characteristics, 44.6% of the patients reported chest pain upon breathing and 32.1% reported retrosternal pain. The same evaluation performed in the infirmary, during the immediate postoperative period, ranged from 0 to 10, with a mean of 3.75 ± 0.30, being 69.6% of chest pain upon breathing and 78.6% of retrosternal pain. On postoperative day 7, according to VAS, pain ranged from 0 to 10, with a mean of 2.05 ± 0.31; regarding characteristics, it was continuous in 32.1% of the cases, and retrosternal in 26.8%. On postoperative day 28, pain ranged from 0 to 3, with a mean of 0.17 ± 0.08, 7.1% of mechanical rhythm and 5.4% upper posterior."

Jornal Brasileiro de Pneumologia

Print version ISSN 1806-3713

J. bras. pneumol. vol.34 no.3 São Paulo Mar. 2008

http://www.scielo.br/scielo.php?script=sci_arttext&pid=S1806-37132008000300003&lng=en&nrm=iso&tlng=en

Our data confirmed that sympathectomy in patients with EPH results in a disturbance of bronchomotor tone and cardiac function.

Our study was composed of patients affected by EH, and thus having a dysfunction of sympathetic activity. The observed respiratory and clinical effects would probably not be observed in healthy individuals.

(ii) The cardio-respiratory effects were observed 6 months after operation. However, a longer postoperative period would be required to determine if they are long-term effects.

(iii) The number of patients was too limited, thus our results should be corroborated by larger studies.

CONCLUSION

Our data confirmed that sympathectomy in patients with EPH results in a disturbance of bronchomotor tone and cardiac function.

1. 
   

   Eur J Cardiothorac Surg (2012)

   doi: 10.1093/ejcts/ezs071

1. 
   

Scientists have created a device that can beat arthritis agony - vagus nerve stimulation for arthritis and other disorders

Scientists have created a device that can beat arthritis agony | Health | Life & Style | Daily Express: "Tiny pacemaker-style devices embedded in the necks of patients with chronic rheumatoid arthritis "hacked" into their nervous systems.

The implant fires bursts of electrical impulses into a key nerve that relays brain signals to the body's vital organs.

Scientists, conducting a groundbreaking trial of the implant, say more than half found their condition dramatically improved.

More than 400,000 patients in the UK are affected by the debilitating disease. Now researchers believe the same technique, which can eliminate the need for a daily cocktail of drugs, could reverse conditions like asthma, obesity and diabetes.

The findings, revealed to Sky News, will be published in the new year.

We may be able to achieve remission in 20 to 30 per cent of patients
Paul-Peter Tak, Rheumatologist Professor
More than half the 20 patients taking part in tests at the Academic Medical Centre in Amsterdam have shown significant improvement.

Rheumatologist Professor Paul-Peter Tak said even for those unaffected by the most modern medicines, they saw an improvement.

"We may be able to achieve remission in 20 to 30 per cent of patients - a huge step forward in the treatment of rheumatoid arthritis," he added.

Doctors hope the implant could be widely used within a decade, but concede they do not yet fully understand how it has such a powerful effect. It stimulates the vagus nerve, which connects the brain to major organs.

By firing impulses for just three minutes a day, scientists were able to reduce the activity of the spleen, a key organ in the immune system.

Within a matter of days, the organ produced fewer chemicals and other immune cells that cause the abnormal inflammation in the joints of people with rheumatoid arthritis.

Kris Famm, who is leading the research, said: "I hope that in 10 to 20 years if you or I had diabetes, we would go to the doctor and there is an option for this sort of device."

Patient Monique Robroek was in so much pain she struggled to walk across a room, despite taking the strongest possible arthritis drugs.

She had an implant fitted under her skin a year ago and has now stopped taking medication and is pain free.

"I have my normal life back," she said. "Within six weeks I felt no pain. It is like magic.""



'via Blog this'

Acute pain following needlescope-VATS (nVATS) sympathectomy

"...recently Sihoe et al. [10] have reported that pre-emptive wound infiltration with a local anaesthetic reduces the postoperative wound pain following needlescope-VATS (nVATS) sympathectomy for palmar hyperhidrosis. The concept of pre-emptive analgesia has gained popularity following
experimental work, demonstrating that early control of pain can alter its subsequent evolution as well as the recognition that nociception produces important physiological responses, even in adequately anaesthetised individuals, and the understanding that for many individuals the minimisation of pain can improve clinical outcomes [11].
The pre-emptive analgesia is based on the intuitive idea that if pain is treated before the injury occurs, the nociceptive system will perceive less pain than if analgesia is given after the injury has already occurred. The preoperative administration of analgesic will modify the afferent nociceptive barrage from the site of injury, thus preventing the development of central sensitisation and hyperalgesia [12].
Thus, we have focussed on this argument in the aim of the present study, which is to determine whether pre-emptive local analgesia (PLA) has an effect to reduce acute postoperative pain following standard-VATS (s-VATS) sympathectomy, in view of n-VATS being considered less painful
than the s-VATS procedure [4,5]."

http://ejcts.oxfordjournals.org/content/37/3/588.full.pdf+html
European Journal of Cardio-thoracic Surgery 37 (2010) 588—593
Pre-emptive local analgesia in video-assisted thoracic surgery sympathectomy

Alfonso Fiorelli, Giovanni Vicidomini, Paolo Laperuta, Luigi Busiello,
Anna Perrone, Filomena Napolitano, Gaetana Messina, Mario Santini*
Thoracic Surgery Unit, Second University of Naples, Naples, Italy
Received 28 March 2009; received in revised form 21 July 2009; accepted 31 July 2009; Available online 12 September 2009

"sympathicotomy may cause a temporary impairment of the caudal-to-rostral hierarchy of thermoregulatory control and changes in microcirculation"

Patients with palmar hyperhidrosis have been reported to have a much
more complex dysfunction of autonomic nervous system, involving compensatory high parasympathetic activity as well as sympathetic overactivity (13, 14), suggesting that sympathicotomy initially induces a sympathovagal imbalance with a parasympathetic predominance, and that this is restored on a long-term basis (14). Therefore, thoracic sympathicotomy may cause a temporary impairment of the caudal-to-rostral hierarchy of thermoregulatory control and changes in microcirculation.

The reduction of finger skin temperature on the non-denervated side may be due to either a decrease in the cross-
inhibitory effect or the abnormal control of the inhibitory fibers by the sudomotor center (6).
Vasoconstrictor neurons have been found to be largely under the inhibitory control of various afferent
input systems from the body surface, whereas sudomotor neurons are predominantly under excitatory
control (15). The basic neuronal network for this reciprocal organization is probably located in the spinal level (15). Therefore, the reduction in the contralateral skin temperature may be explained by cross-inhibitory control of various afferent in the spinal cord.
In particular, our study showed that, following bilateral T3 sympathicotomy, the skin temperatures on
the hands increased whereas the skin temperatures on the feet decreased. These findings suggest a
cross-inhibitory control between the upper and lower extremities. However, the pattern of skin
temperature reduction on the feet differed from that on the contralateral hand. The skin temperature on
the feet did not decrease after right T3 sympathicotomy but decreased significantly after bilateral T3
sympathicotomy.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2722005/

Effect of ganglion blockade on cerebrospinal fluid norepinephrine

Prevention of ganglion blockade-induced hypotension using phenylephrine did not prevent the decrease in CSF NE caused by trimethaphan, and when phenylephrine was discontinued, the resulting hypotension was not associated with increases in CSF NE. The similar decreases in plasma NE and CSF NE during ganglionic blockade, and the abolition of reflexive increases in CSF NE during hypotension in ganglion-blocked subjects, cast doubt on the hypothesis that CSF NE indicates central noradrenergic tone and are consistent instead with at least partial derivation of CSF NE from postganglionic sympathetic nerve endings.

 http://www.mendeley.com/research/effect-of-ganglion-blockade-on-cerebrospinal-fluid-norepinephrine/

"sympathectomy, although having varying results, does seem to increase the severity of autoimmune disorders"

Allostasis - a state of imbalance responsible for Autoimmune disorders

In general, enhancing the sympathetic tone decreases both T0-cell and NK cell functions but not the proliferation of splenic B cells (Dowdell and Whitacre, 2000). In contrast, chemical sympathectomy, although having varying results, does seem to increase the severity of autoimmune disorders (Dowdell and Whitacre, 2000)
As far as metabolism, catecholamines promote mobilization of fuel stores at time of stress and act synergistically with glucocorticoids to increased glycogenolysis, gluconeogenesis, and lipolysis but exert opposing effects of protein catabolism, as noted earlier. One important aspect is regulation of body temperature (Goldstein and Eisenhofer, 2000) Epinephrine levels are also positively related to serum levels of HDL cholesterol and negatively related to triglycerines. However, perturbing the balance of activity of various mediators or metabolism and body weight regulation can lead to well-known metabolic disorders such as type 2 diabetes and obesity.

At the same time, increased sympathetic activitation and nerephinephrine release is elevated in hypertensive individuals and also higher levels of insulin, and there are indications that insulin further increases sympathetic activity in a vicious cycle (Arauz-Pacheco et al.,1996)

As a result of either local production, cytokines often enter the the circultion and can be detected in plasma samples. Sleep deprivation and psychological stress, such as public speaking, are reported to elevate inflammatory cytokine level in blood (Altemus et al., 2001) Circulting levels of a number of inflammatory cytokines are elevated in relation to viral and other infections and contirbute to the feeling of being sick, as well as sleepiness, wiht both direct and indirect effects on the central nervous system (Arkins et al., 2000; Obal and Kueger, 2000)

Inflammatory autoimmune diseases, such as multiple sclerosis, rheumatoid arthritis, and type 1 diabetes, reflect an allostatic state that consists of at least three principal causes: genetic risk factors, (...) factors that contribute to the development of tolerance of self-antigens (...) and the hormonal mikieu that regulates adaptive immunes responses (Dowdell and Whitacre, 2000)

Allostasis, homeostasis and the costs of physiological adaptation

By Jay SchulkinCambridge University Press, 2004

Allostasis is the process of achieving stability, or homeostasis, through physiological or behavioral change. This can be carried out by means of alteration in HPA axishormones, the autonomic nervous system, cytokines, or a number of other systems, and is generally adaptive in the short term ^[1]

24-hour melatonin measurements in normal subjects and after peripheral sympathectomy

J Clin Endocrinol Metab. 1991 Apr;72(4):819-23.

Sequential cerebrospinal fluid and plasma sampling in humans: 24-hour melatonin measurements in normal subjects and after peripheral sympathectomy.

Bruce J1, Tamarkin L, Riedel C, Markey S, Oldfield E.

Abstract

Simultaneous measurements of plasma and cerebrospinal fluid (CSF) melatonin and urinary excretion of 6-hydroxymelatonin were performed in four normal volunteers and one patient before and after upper thoracic sympathectomy for the control of essential hyperhidrosis. For normal individuals, hourly 24-h melatonin concentrations in plasma and CSF exhibited similar profiles, with low levels during the day and high levels at night. Peak plasma levels varied from 122-660 pmol/L, and the peak CSF levels from 94-355 pmol/L. The onset of the nocturnal increase in melatonin did not occur at the same time for each individual. Urinary 6-hydroxymelatonin levels also exhibited a daily rhythm, with peak excretion at night. The individual with the lowest nocturnal levels of circulating melatonin also had the lowest excretion of 6-hydroxymelatonin. In the patient with hyperhidrosis, a prominent melatonin rhythm was observed preoperatively in the CSF and plasma. After bilateral T1-T2 ganglionectomy, however, melatonin levels were markedly reduced, and the diurnal rhythm was abolished. These results provide direct evidence in humans for a diurnal melatonin rhythm in CSF and plasma as well as regulation of this rhythm by sympathetic innervation.

http://www.ncbi.nlm.nih.gov/pubmed/2005207

Ablation of the sympathetic nervous system by sympathectomy is a standard model for the study of sympathetic nervous system regulation of immune function

Ablation of the sympathetic nervous system by chemical sympathectomy is a standard model for the study of sympathetic nervous system regulation of immune function. We have previously documented that chemical denervation results in enhanced antigen-specific, but suppressed mitogen-induced, cytokine production by spleen cells. In our investigation into the mechanisms ofsympathectomy-induced immune alterations, we first evaluated the peritoneal environment into which the protein antigen keyhole limpet hemocyanin is administered. Denervation resulted in increased production of tumor necrosis factor- by peritoneal exudate cells and these cells appeared to have enhanced antigen presenting capability. We hypothesized that nerve terminal destruction may be inducing an inflammatory response by monocyte/macrophages and other cell types throughout the periphery that could differentially alter subsequent mitogen versus antigen-specific responses. However, no evidence of sympathectomy-induced systemic or local splenic inflammatory responses was observed, as indicated by measuring the proinflammatory cytokines tumor necrosis factor- and interleukin-1. These experiments indicate that an inflammatory response is not likely to be responsible for sympathectomy-induced immune alterations, eliminating a potential confounding factor in interpreting sympathectomy studies.Copyright 2001 Elsevier Science (USA).

Authors: Callahan T.A.^{1, 2}; Moynihan J.A.^{1, 2, 3, 4, 5}
Source: Brain, Behavior, and Immunity, Volume 16, Number 1, February 2002 , pp. 33-45(13)

The biology and control of surface overhealing

Lesions of “surface overhealing” include keloid, hypertrophic scar, and burn scar. All are characterized by overabundant collagen deposition. The biology of these lesions is reviewed, suggesting that abnormal collagen metabolism results from alterations in the inflammatory/immune response. Practical and theoretical treatment plans are outlined based on methods that alter collagen metabolism, the inflammatory/immune system or rely on physical alterations (surgery, pressure).

http://www.springerlink.com/content/3g2mr5r32m438125/

RA, lupus and other connective tissue disorders may have abnormalities of sympathetic postganglionic function

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.
http://www.emedicine.com/NEURO/topic720.htm

The sympathetic nervous system stimulatesanti-inflammatory B cells in collagen-type II-inducedarthritis

Ann Rheum Dis 2012;71:432–439. doi:10.1136/ard.2011.153056 

Removal of noradrenergic innervation by sympathectomy enhanced the severity of symptoms in EAE

Sympathetic regulation of Autoimmune Disease

In animal models of human autoimmune disease, alterations in sympathetic innervation, NE concentration and lymphocyte AR expression have been demonstrated. ....reduced splenic noradrenergic innervation and decreased splenic NE concentration were apparent before the onset os disease symptoms. In myelin basic protein-induced EAE and MS-like disease, a reduction in splenic NE concentration was reported at the time of maximal antigen-induced lymphocyte proliferation and was accompanied by an increase in the density of of splenic lymphocyte beta-AR. In chronic/relapsing EAE (CREAE) induced in rats, splenocyte beta-AR density correlated positively with the severity of CREAE. Removal of noradrenergic innervation by chemical sympathectomy with 6-OHDA enhanced the severity of symptoms in EAE...

Neuropsychiatry  By Randolph B. Schiffer, Stephen M. Rao, Barry S. Fogel Published 2003 Lippincott Williams & Wilkins

Alterations in T and B cell proliferation

Functional changes in lymph node (LN) and spleen lymphocytes were examined following sympathetic denervation of adult mice with 6-hydroxydopamine (6-OHDA). Sympathectomy reduced in vitro proliferation to concanavalin A (ConA) by LN cells and decreased LN Thy-1+ and CD4+ T cells. At the same time, ConA-induced interferon-gamma (IFN-gamma) production was increased, but interleukin-2 (IL-2) production was not altered. After sympathectomy, lipopolysaccharide (LPS)-stimulated proliferation of LN B cells was enhanced, in parallel with an increase in the proportion of sIgM+ cells. LPS-induced polyclonal IgM secretion was decreased, whereas polyclonal IgG secretion was dramatically enhanced. In the spleen, ConA and LPS responsiveness was reduced after sympathectomy, as was IL-2 and IFN-gamma production. The decreased proliferation was not associated with changes in splenic T and B cell populations. The uptake blocker desipramine prevented the 6-OHDA-induced changes in spleen and LN, indicating that these alterations were dependent upon neuronal destruction. These results provide evidence for heterogeneity of sympathetic nervous system regulation of T and B lymphocyte function and for organ-specific influences on immune function.
http://www.researchgate.net/publication/14903863_Sympathetic_nervous_system_modulation_of_the_immune_system._III._Alterations_in_T_and_B_cell_proliferation_and_differentiation_in_vitro_following_chemical_sympathectomy

Sympathectomy decreased CD4+ T-cells in lymph nodes - Sympathetic denervation leads to loss of an important regulatory mechanism in immune system physiology

Sympathectomy decreased CD4+ T-cells in lymph nodes.
Alterations in lymphocyte activity does not always correlate with changes in the proportions of T- or B-lymphocyte subsets. Sympathetic denervation leads to loss of an important regulatory mechanism in immune system physiology. This is apparently site specific in that both lymph node and spleen T-cell proliferative responses are reduced.
Article by Dr. Brian A. Smith
http://home.earthlink.net/~doctorsmith/hivandchiro.htm

Patients with surgical sympathectomies have low plasma levels of DA and NE [49], whereas EPI:NE ratios are increased

Patients with surgical sympathectomies have low plasma levels of DA and NE [49], whereas EPI:NE ratios are increased (unpublished observations), suggesting decreased sympathetically mediated exocytosis and compensatory adrenomedullary activation.

Catecholamines 101, David S. Goldstein
Clin Auton Res (2010) 20:331–352

The mechanisms by which sympathectomy leads to increased local bone loss is unknown

In vivo effects of surgical sympathectomy on intra... [Am J Otol. 1996] - PubMed - NCBI: "Am J Otol. 1996 Mar;17(2):343-6.

In vivo effects of surgical sympathectomy on intramembranous bone resorption.
Sherman BE1, Chole RA.
Author information
1Department of Otolaryngology--Head and Neck Surgery, School of Medicine, University of California, Davis, USA.
Abstract
Bone modeling and remodeling are highly regulated processes in the mammalian skeleton. The exact mechanism by which bone can be modeled at a local site with little or no effect at adjacent anatomic sites is unknown. Disruption of the control of modeling within the temporal bone may lead to various bone disease such as otosclerosis, osteogenesis imperfecta, Paget's disease of bone, fibrous dysplasia, or the erosion of bone associated with chronic otitis media. One possible mechanism for such delicate control may be related to the ubiquitous and rich sympathetic innervation of all periosteal surfaces. Previous studies have indicated that regional sympathectomy leads to qualitative alterations in localized bone modeling and remodeling. In this study, unilateral cervical sympathectomy resulted in significant increases in osteoclast surface and osteoclast number within the ipsilateral bulla of experimental animals. The mechanisms by which sympathectomy leads to increased local bone loss is unknown. Potential mechanisms include disinhibition of resorption, secondary to the elimination of periosteal sympathetics, as well as indirect vascular effects."

after sympathectomy "He becomes more quiet, less impressionable, less agitated, tremor diminishes..."

Everyone seems to agree that when sympathectomy is successful the subjective symptoms of the patient show a considerable improvement. He becomes more quiet, less impressionable, less agitated, tremor diminishes, tachycardia, however, is little influenced or not at all, and the same is true for goiter.
   In conclusion it may be said that the results obtained from sympathectomy when present are very immediate. The ocular symptoms are the ones most happily influenced by the operation; the others such as nervousness, tachycardia, and goiter are problematical.
   Remote Results.- In going over the cases operated by Jaboulay as far back as twelve and fourteen years, A. Charlier was able to find that a number of his patients had been cured completely. He was able to retrace 18 out of the 31 cases operated by Jaboulay from four to fourteen years before. Three of them were completely cured, 9 of them were so ameliorated that the subjective cure was a complete one, the objective cure, however, being incomplete; the 6 remaining cases were doubtful. All these patients experienced considerable benefit to their nervous symptoms; improved and no trophic disturbances of any sort followed as the result of sympathectomy.

Title	Thyroid and Thymus
Author	André Crotti
Publisher	Lea & Febiger, 1918
Original from	Harvard University
Digitized	17 Dec 2007
Length	567 pages