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).

Sympathectomy - a neurocardiologic disorder

Bilateral thoracic sympathectomies or sympathotomies are done for refractory palmar hyperhidrosis [85–87]. Iontophoresis, botulinum toxin injection, and glycopyrrolate cream are alternatives. Because sweating is mediated mainly by sympathetic cholinergic fibers, autonomic neurosurgery is usually effective; however, a variety of expected and unexpected consequences can result, including ectopic (e.g., plantar) hyperhidrosis, gustatory sweating, Horner syndrome, and decreased heart rate responses to exercise. The latter seems to be related to partial cardiac denervation [88]. Anecdotally, fatigue, altered mood, blunted emotion, and decreased ability to concentrate can develop after bilateral thoracic sympathectomies. 

β-Adrenoceptor blockers are a mainstay of treatment for CPVT. An automated defibrillator may have to be implanted. Treatment for CPVT also includes left sympathectomy. Such treatment leaves open the theoretical possibilities of denervation supersensitivity of cardiac adrenoceptors and compensatory activation of the adrenomedullary hormonal system; however, plasma levels of catecholamines have not been assessed in CPVT with or without therapeutic cardiac denervation.

Table 1. Neurocardiologic disorders that feature abnormal catecholaminergic function

Disorders where abnormal catecholaminergic function is etiologic Hypofunctional states without central neurodegeneration
Acute, primary
Neurocardiogenic syncope Spinal cord transection Acute pandysautonomia Sympathectomy
Acute, secondary
Drug-related (e.g., alcohol, tricyclic antidepressant, chemotherapy, opiate, barbiturates, benzodiazepines, sympatholytics, general anesthesia)
Seizures
Guillain–Barre syndrome Alcohol

Chronic, primary

Pure autonomic failure
Horner's syndrome
Familial dysautonomia
Carotid sinus syncope

Adie's syndrome Dopamine-β-hydroxylase deficiency
Sympathectomy 

http://onlinelibrary.wiley.com/doi/10.1111/j.1755-5922.2010.00244.x/full

https://archive.is/UMW1w

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.

Patients may develop bradycardia after surgical procedure to treat sweaty hands and blushing

Upper-Thoracic Sympathectomy; Patients may develop bradycardia after surgical procedure

Heart Disease Weekly. Atlanta: Feb 23, 2003. pg. 71

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

Sympathectomy at T2 leads to decreased negative feedback to the hypothalamus

Compensatory sweating was originally thought to be a mechanism of excessive sweating (in an anatomical region with an intact sympathetic nervous system) to maintain a constant rate of total sweat secretion.90 However, this theory was not confirmed by other studies, demonstrating that compensatory sweating represented a reflex action by an altered feedback mechanism at the level of the hypothalamus which is dependent on the level at which sympathetic denervation occurs. Sympathectomy at the level of the T2 ganglion leads to decreased negative feedback to the hypothalamus. When performing a sympathectomy at a lower level, the negative feedback to the hypothalamus is less inhibited, leading to a decrease in compensatory sweating. Chou et al.91 have proposed the term ‘reflex sweating’ to replace compensatory sweating. Other side effects described in a review article by Dumont89 are gustatory sweating, cardiac effects, phantom sweating, lung function changes, dry hands and altered taste. Besides these side effects there are significant risks of complications during and after surgery (arterial or venous vascular injury, pneumothorax, infection, Horner syndrome etc.).

JEADV 2012, 26, 1–8 Journal of the European Academy of Dermatology and Venereology

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

Acta Physiol Scand. 2000 Sep;170(1):33-8.

Middle cerebral artery blood velocity during exercise with beta-1 adrenergic and unilateral stellate ganglion blockade in humans.

Ide K1, Boushel R, Sørensen HM, Fernandes A, Cai Y, Pott F, Secher NH.

Author information

Abstract

A reduced ability to increase cardiac output (CO) during exercise limits blood flow by vasoconstriction even in active skeletal muscle. Such a flow limitation may also take place in the brain as an increase in the transcranial Doppler determined middle cerebral artery blood velocity (MCA V(mean)) is attenuated during cycling with beta-1 adrenergic blockade and in patients with heart insufficiency. We studied whether sympathetic blockade at the level of the neck (0.1% lidocaine; 8 mL; n=8) affects the attenuated exercise - MCA V(mean following cardio-selective beta-1 adrenergic blockade (0.15 mg kg(-1) metoprolol i.v.) during cycling. Cardiac output determined by indocyanine green dye dilution, heart rate (HR), mean arterial pressure (MAP) and MCA V(mean) were obtained during moderate intensity cycling before and after pharmacological intervention. During control cycling the right and left MCA V(mean) increased to the same extent (11.4 +/- 1.9 vs. 11.1 +/- 1.9 cm s(-1)). With the pharmacological intervention the exercise CO (10 +/- 1 vs. 12 +/- 1 L min(-1); n=5), HR (115 +/- 4 vs. 134 +/- 4 beats min(-1)) and delta MCA V(mean) (8.7 +/- 2.2 vs. 11.4 +/- 1.9 cm s(-1) were reduced, and MAP was increased (100 +/- 5 vs. 86 +/- 2 mmHg; P < 0.05). However, sympathetic blockade at the level of the neck eliminated the beta-1 blockade induced attenuation in delta MCA V(mean) (10.2 +/- 2.5 cm s(-1)). These results indicate that a reduced ability to increase CO during exercise limits blood flow to a vital organ like the brain and that this flow limitation is likely to be by way of the sympathetic nervous system.

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

Sympathectomy and parasympathectomy leads to the hyperfunction of the serotoninergic system and pathology

We studied the balance of activity of sympathetic, parasympathetic, and serotoninergic divisions of the autonomic nervous system in the regulation of the heart function in rabbits. High activities of the sympathetic and parasympathetic system are associated with antagonistic interactions between them. Moderation of activity of these systems could be accompanied by activation of the serotoninergic system. Physiological sympathectomy and parasympathectomy lead to hyperfunction of the serotoninergic system and pathology.

Bulletin of Experimental Biology and Medicine, Vol. 140, No. 5, 2005 PHYSIOLOGY

Disturbances in brain serotonergic systems result in a range of phenotypes such as depression, suicide and anxiety disorders.

http://www.biomedcentral.com/1471-2202/10/50

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

Swelling and oedema is often observed in patients after acute interruption of post-ganglionic sympathetic fibres such as a wide-spread sympathectomy

Swelling and oedema is often observed in patients with Raynaud's disease or causalgia after acute interruption of post-ganglionic sympathetic fibres such as a wide-spread sympathectomy. Complete sympathetic block dilates vein and capillary and increases peripheral pooling, which raises hydrostatic the shins and feet (fig 2), constipation and abdominal distention, and dysuria were observed. Oedema was not noted in the hands or face. There were no signs or abnormal laboratory data suggesting heart failure, renal failure, liver dysfunction, thyroid dysfunction or local inflammation. Venography of the left leg did not show obstruction in the deep veins.

We showed that the preganglionic sympathetic tract in the spinal cord was often disturbed in patients with multiple sclerosis with myelopathy.' Most patients with complete transection of the spinal cord due to injury showed swelling of the lower limbs or oedema, but they gradually subsided within several months even without restoration of somatic function. Probably some compensatory mechanism improves the hydrostatic condition in the chronic stage and explains why oedema is not noted in patients with chronic autonomic failure syndrome.
Journal of Neurology, Neurosurgery, and Psychiatry 1992;55:232-239

http://jnnp.bmj.com/content/55/3/232.1.full.pdf

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

peripheral sympathectomy causes a dramatic increase in NGF levels in the denervated organs

Increased Nerve Growth Factor Messenger RNA and Protein

Peripheral NGF mRNA and protein levels following
sympathectomy
It has been shown previously that peripheral sympathectomy
causes a dramatic increase in NGF levels in the denervated
organs (Yap et al., 1984; Kanakis et al., 1985; Korsching and
Thoenen, 1985).
Increased ,&Nerve Growth Factor Messenger RNA and Protein
Levels in Neonatal Rat Hippocampus Following Specific Cholinergic
Lesions
Scott R. Whittemore,” Lena Liirkfors,’ Ted Ebendal,’ Vicky R. Holets, 2,a Anders Ericsson, and HBkan Persson
Departments of Medical Genetics and’ Zoology, Uppsala University, S-751 23 Uppsala, Sweden, and *Department of
Histology, Karolinska Institute, S-104 01 Stockholm, Sweden

Sympathectomy reduces emotional, stress-induced sweating indicating that it affects the stress-response

"...for reasons that are not obvious, many patients with facial hyperhidrosis and hyperhidrosis of the feet will benefit from upper thoracic sympathectomy. " 

(The Journal of Pain, Vol 1, No 4 (Winter), 2000: pp 261-264)

"Bilateral upper thoracic sympathicolysis is followed by redistribution of body perspiration, with a clear decrease in the zones regulated by mental or emotional stimuli, and an increase in the areas regulated by environmental stimuli, though we are unable to establish the etiology of this redistribution." 

(Surg Endosc. 2007 Nov;21(11):2030-3. Epub 2007 Mar 13.) 


"Palmar hyperhidrosis of clinical severity is a hallmark physical sign of many anxiety disorders, including generalized anxiety disorder, panic disorder, posttraumatic stress disorder, and especially social phobia.4 These are increasingly well understood and highly treatable neurobiological conditions. They are mod- erately heritable hard-wired fear responses,5 and are linked to amygdalar and locus coeruleus hyper-reactivity during psycho- social stress.6,7 Anxiety disorders are known to be much more common among women. This is consistent with the finding of Krogstad et al. that among controls sweating was reported more often by men, while among the hyperhidrosis group sweating was reported more often among women."

"A surgical treatment for anxiety-triggered palmar hyperhidrosis is not unlike treating tearfulness in major depression by severing the nerves to the lacrimal glands. We have recently made a similar argument advocating a psychopharmacological, rather then a surgi- cal, first-line treatment for blushing.9" 
(Journal Compilation - 2006 British Association of Dermatologists - British Journal of Dermatology 2006, DOI: 10.1111/j.1365-2133.2006.07547.x
 )

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

Eur J Appl Physiol. 2004 Oct;93(1-2):245-51. Epub 2004 Aug 25.

Infrared thermography for examination of skin temperature in the dorsal hand of office workers.

Gold JE1, Cherniack M, Buchholz B.

Reduced blood flow may contribute to the pathophysiology of upper extremity musculoskeletal disorders (UEMSD), such as tendinitis and carpal tunnel syndrome. The study objective was to characterize potential differences in cutaneous temperature, among three groups of office workers assessed by dynamic thermography following a 9-min typing challenge: those with UEMSD, with ( n=6) or without ( n=10) cold hands exacerbated by keyboard use, and control subjects ( n=12). Temperature images of the metacarpal region of the dorsal hand were obtained 1 min before typing, and during three 2-min sample periods [0-2 min (early), 3-5 min (middle), and 8-10 min (late)] after typing. Mean temperature increased from baseline levels immediately after typing by a similar magnitude, 0.7 (0.3) degrees C in controls and 0.6 (0.2) degrees C in UEMSD cases without cold hands, but only by 0.1 (0.3) degrees C in those with cold hands. Using paired t-tests for within group comparisons of mean dorsal temperature between successive imaging periods, three patterns of temperature change were apparent during 10 min following typing. Controls further increased mean temperature by 0.1 degrees C ( t-test, P=0.001) at 3-5 min post-typing before a late temperature decline of -0.3 degrees C ( t-test, P=0.04), while cases without cold hands showed no change from initial post-typing mean temperature rise during middle or late periods. In contrast, subjects with keyboard-induced cold hands had no change from initial post-typing temperature until a decrease at the late period of -0.3 degrees C ( t-test, P=0.06). Infrared thermography appears to distinguish between the three groups of subjects, with keyboard-induced cold hand symptoms presumably due, at least partially, to reduced blood flow.

http://www.ncbi.nlm.nih.gov/pubmed/15338221

cervical sympathectomy induces mast cell hyperplasia and increases histamine and serotonin content in the rat 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