Effects of Sympathectomy on the mean decrease in HBF (Hypothalamic blood flow)

Intrahypothalamic injection of 0.1 mug of tyramine caused a mean decrease in HBF of 15.6 ml/100 g per min (P less than 0.001). This effect of intrahypothalamic injection of tyramine was abolished by bilateral cervical sympathectomy but not by chemical sympathectomy of the upper brainstem. These results support the idea that local CBF, at least in the hypothalamus, is mediated by two distinct pathways. The first consists of the sympathetic nerves which arise in the cervical ganglia, and which activate intrahypothalamic alpha-receptors to cause constriction. The second is an entirely intracerebral noradrenergic pathway which stimulates beta-receptors to cause vasodilation.
http://circres.ahajournals.org/cgi/content/abstract/circresaha;38/3/140
Circulation Research, Vol 38, 140-145, Copyright © 1976 by American Heart Association

Cutaneous vasodilator responses induced by activation of hypothalamic heat loss mechanisms are completely abolished by sympathectomy

http://www3.interscience.wiley.com/journal/121531565/abstract

sympathectomy significantly increased the ratio of patients exhibiting a positive response to methacholine

Of 46 patients who had a negative result for methacholine challenge preoperatively, 12 (26%) became positive after surgery. In terms of the level of sympathectomy, T3 sympathectomy significantly increased the ratio of patients exhibiting a positive response to methacholine (from 19% to 34%, respectively) (p < 0.005).
Conclusions. Thoracic sympathectomy can adversely affect lung function early after surgery, although the clinical significance is uncertain. It may also exert an influence on the development of bronchial hyperresponsiveness, especially when performed at the T3 level.
Journal of Asthma, 46:276–279, 2009

Evidence: sympathectomy created imbalance of autonomic activity and functional changes of the intrathoracic organs

Surgical thoracic sympathectomy such as ESD or heart transplantation can result in an imbalance between the sympathetic and parasympathetic activities and result in functional changes
in the intrathoracic organs.
Therefore, the procedures affecting sympathetic nerve functions, such as epidural anesthesia, ESD, and heart transplantation, may cause an imbalance between sympathetic and parasympa-
thetic activities (1, 6, 16, 17). Recently, it has been reported that ESD results in functional changes of the intrathoracic organs.


In conclusion, our study demonstrated that ESD adversely affected lung function early after surgery and the BHR was affected by an imbalance of autonomic activity created by bilateral ESD in patients with primary focal hyperhidrosis.
Journal of Asthma, 46:276–279, 2009

THE SYMPATHETIC NERVOUS SYSTEM AS A HOMEOSTATIC MECHANISM

The responses of intact rats to cold-exposure (4°C) include vasoconstriction, piloerection, shivering, adrenocorticotrophin (ACTH) hypersecretion and increased mobilization of free fatty acids and glucose. Adrenal demedullation prevents the increased mobilization of glucose and decreases survival time. Chemical sympathectomy blocks all of the responses except ACTH hypersecretion. Such animals lose body heat rapidly and die in a few hours. Total adrenalectomy has a similar effect. The damaging actions of chemical sympathectomy are reversed by administration of catecholamines while those of total adrenalectomy are reversed by cortisone. Thus, the sympathetic nervous system appears to be essential for existence at low environmental temperature.

http://jpet.aspetjournals.org/cgi/content/abstract/157/1/103

Pathophysiology of Diarrhea and Malabsorption

Disordered motility

• Post-vagotomy

• Post-sympathectomy

• Diabetic neuropathy

• Hyperthyroidism

• Addison’s disease (adrenal insufficiency)

• Irritable bowel syndrome

Laurence Scott Bailen, M.D.: Diarrhea and Malabsorption
http://ocw.tufts.edu/Content/48/lecturenotes/571075

Response to adrenaline after sympathectomy

None of the hands in this series
exhibited significant change in flow with A1 ,ug/min. With A ,ug/min, however,
eight of the thirteen hands now had 25 % or more vasoconstriction, the mean
for the group being 30 %. With i p,g no less than eight of the ten hands tested
had more than 25 % vasoconstriction.
Thus for the two groups receiving H and i ug adrenaline marked increases
in the mean responses from 11 to 30 % and from 16 to 44 %, respectively, were
observed after sympathectomy. The ratio of postoperative to preoperative
mean responses was about the same for both doses (2-7 and 2-8). The increased
response after sympathectomy is seen (Table 2) to be due especially to changes
in hands 3, 6, 9, 11, 12 and 13, which before operation had minimal constric-
tions but responded with marked reductions in blood flow after sympathectomy.
The altered behaviour of two of these hands is portrayed in Figs. 1 and 2.
Although some of the other seven hands also showed increased vasoconstric-
tion with a given dose of adrenaline after sympathectomy this increase was
less notable.
The paired differences between the hands before and after sympathectomy
are significant at the A .g/min (t = 3-03, P < 0-02), and the i ,ug/min (t = 3-55,
P < 0-01) levels. Of the six hands manifesting notable increases in sensitivity
to adrenaline three were sympathectomized by preganglionic section and three
by ganglionectomy.
J. Physiol. (I955) I29, 53-64
EFFECT OF ADRENALINE AND NORADRENALINE ON
BLOOD VESSELS OF THE HAND BEFORE AND AFTER
SYMPATHECTOMY
BY R. S. DUFF
From the Cardiological Department, St Bartholomew's Hospital and the
Sherrington School of Physiology, St Thomas's Hospital, London

Intraneural activated T cells cause focal breakdown of the blood-nerve barrier

These findings demonstrate that activated T cells cause focal breakdown of the BNB, allowing circulating antimyelin antibody to enter the endoneurium with consequent focal demyelination.
Brain. 1995 Aug;118 ( Pt 4):857-68
Intraneural activated T cells cause focal breakdown of the blood-nerve barrier.

Spies JM, Westland KW, Bonner JG, Pollard JD.
Institute of Clinical Neurosciences, University of Sydney, NSW Australia.

Immune and Glial Cells Contribute to Pathological Pain States

Alterations in sympathetic fibers rapidly follow peripheral nerve injury. This occurs as sprouting of sympathetic fibers, creating aberrant communication pathways from the new sympathetic terminals to sensory neurons (35). Sympathetic sprouting has been documented in the region of peripheral terminal fields of sensory neurons (262), at the site of nerve trauma (57), and within the dorsal root ganglia (DRG) containing cell bodies of sensory neurons (248, 343). Each of these sites develops spontaneous activity and sensitivity for catecholamines and sympathetic activation (8, 53).
The clearest evidence that immune activation participates in sympathetic sprouting comes from studies of the DRG. DRG cells receive signals that peripheral nerve injury has occurred via retrograde axonal transport from the trauma site. These retrogradely transported signals trigger sympathetic nerve sprouting
into DRG (205, 308). As a result of nerve damage-induced retrogradely transported signals, glial cellswithin the DRG (called satellite cells) proliferate and become activated; macrophages are
recruited to the DRG as well. In turn, the activated satellite glial cells (and, presumably, the
macrophages) release proinflammatory cytokines and a variety of growth factors into the extracellular fluid of the DRG (206, 246-248, 258, 277, 308, 358). These substances stimulate and direct the growth of sympathetic fibers, which form basket-like terminals around the satellite cells that, in turn, surround neuronal cell bodies.
Physiological Reviews, Vol. 82, No. 4, October 2002, pp. 981-1011; 10.1152/physrev.00011.2002.
Copyright ©2002 by the American Physiological Society

Sympathectomy induces mast cell hyperplasia and chronic inflammation

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.
http://www.ncbi.nlm.nih.gov/pubmed/11919420

Long-term superior cervical sympathectomy induces mast cell hyperplasia and increases histamine and serotonin content in the rat dura mater
Copyright © 1999 IBRO. Published by Elsevier Science Ltd.

Cervical sympathectomy affects adrenocorticotropic hormone and thyroid-stimulating hormone

The present results suggest that cervical sympathectomy in the rat increases ACTH secretion and decreases TSH secretion in the pituitary. These effects seem to be due to a mildly increased secretion of melatonin in the pineal body that probably in turn increases corticotropin-releasing factor (CRF) secretion and decreases thyrotropin-releasing hormone (TRH) secretion in the hypothalamus. Extrapolation of these findings to humans suggests that longterm and repeated stellate ganglion block would affect the pituitary secretions of ACTH and TSH.
http://www.springerlink.com/content/g3333g7752201496/

Received: 26 June 1995 Accepted: 1 March 1996

Journal of Anesthesia

Hyperpigmentation after sympathectomy

Clinical and Experimental Dermatology

Volume 5 Issue 3, Pages 349 - 350
Accepted for publication 4 October 1979

Abnormal suntanning following transthoracic endoscopic sympathectomy Transthoracic endoscopic sympathectomy (TES) has become the method of choice for treating patients with palmar hypcrhidrosis. There are few complications reported with this procedure. A complication not described previously is reported here. Accepted: 25 January 1996

M. S. Whiteley, S. B. Ray-Chaudhuri, Mr R. B. Galland *

British Journal of Surgery Volume 83 Issue 12, Page 1782

Cytokines, immune responses and depression

There is now evidence that major depression is accompanied by significant changes in cell-mediated and humoral immunity, and these changes may be related to the pathophysiology or pathogenesis of that illness (Connor and Leonard [1], Dantzer et al. [2], Kim et al. [3], Licinio and Wong [4]), yet data are inconsistent. Some studies have shown that major depression is associated with dysregulation of immune mediators.
However, conflicting results have also been described (Brambilla and Maggioni [12], Brambilla et al. [13], Carpenter et al. [14], Rothermundt et al. [15]). These changes have been considered in terms of the imbalance between individual pro- and anti-inflammatory cytokines and the T helper 1 (Th1) and T helper 1 (Th2) imbalance in major depression. On the other hand, an enhanced secretion of such proinflammatory cytokines would not only lead to activation of T and B lymphocytes, but also could affect the brain and elicit various symptoms of depression, such as loss of appetite, listlessness, and sleep disturbances (Maes [16]).

Cytokines, stress and depressive illness

Cytokines, signaling molecules of the immune system, have been implicated as a contributing factor for mood disorders such as depression. Several lines of evidence supporting this contention are briefly reviewed and caveats are introduced. Essentially, a relationship between cytokines and depression is based on the findings that: 1) proinflammatory cytokines (interleukin-1, interleukin-6, tumor necrosis factor-alpha) and bacterial endotoxins elicit sickness behaviors (e.g., fatigue, soporific effects) and symptoms of anxiety/depression that may be attenuated by chronic antidepressant treatment, 2) cytokines induce neuroendocrine and central neurotransmitter changes reminiscent of those implicated in depression, and these effects are exacerbated by stressors, 3) severe depressive illness is accompanied by signs of immune activation and by elevations of cytokine production or levels, and 4) immunotherapy, using interleukin-2 or interferon-alpha, promotes depressive symptoms that are attenuated by antidepressant treatment. It is argued that cytokine synthesis and release, elicited upon activation of the inflammatory response system, provoke neuroendocrine and brain neurotransmitter changes that are interpreted by the brain as being stressors, and contribute to the development of depression. Furthermore, such effects are subject to a sensitization effect so that a history of stressful experiences or cytokine activation augment the response to later challenges and hence the evolution of depression.

Anisman H, Merali Z.
Institute of Neurosciences,
Carleton University and Institute of Mental Health Research,
Royal Ottawa Hospital, University of Ottawa, Canada.
hanisman@ccs.Carleton.ca
Ann Med 2003;35(1):2-11

Sympathectomy-induced changes is cytokine production and immune effector function

Lacrimal Gland, Tear Film, and Dry Eye Syndromes 2: Basic Science and Clinical Relevance

By David D. Sullivan, Darlene A. Dartt, Michele A. Meneray

Edition: 2, illustrated

Published by Springer, 1998

ISBN 0306458128, 9780306458125

significantly more cholesterol and total lipids in the aorta after sympathectomy

While the vasomotor effect of the sympathetic nervous system (SNS) on the arterial wall is well recognized, its trophic function is not. It is the aim of these studies to demonstrate this all-important function as it relates to the vascular muscle.

Although the exact mechanism by which sympathetic nerve impulses influence the metabolism of the vessel wall is unknown, effects of sympathectomy can be demonstrated. Several lines of evidence indicate that chronic absence of sympathetic innervation in rabbits increases collagen synthesis and decreases activity of tricarboxylic acid cycle enzymes in the vascular wall. When chemically sympathectomized rabbits were fed a 1% cholesterol dietary supplement for 80 days, the aortas of these rabbits contained significantly more cholesterol and total lipids than those from fully innervated controls in spite of insignificant differences in plasma lipids.

In a subsequent series of experiments we analyzed the efficacy of the SNS in two strains of pigeons. White Carneau (WC) pigeons are known by their susceptibility to atherosclerosis of the aorta while Show Racer (SR) pigeons are not. Our results demonstrate that the abdominal aorta of WC pigeons has less sympathetic innervation and it declines faster with age than that of SR pigeons. The results of the described studies documenting the direct trophic influence of the SNS on the arterial wall are reinforced by the similarity to the vessel wall changes induced by partial sympathectomy and natural aging.

Trophic effect of the sympathetic nervous system on vascular smooth muscle

	Annals of Biomedical Engineering
	Springer Netherlands
ISSN	0090-6964 (Print) 1573-9686 (Online)
Issue	Volume 11, Number 6 / November, 1983

increased sensitivity to catecholamines due to sympathetic denervation

Concepts related to the pathophysiology of reflex sympathetic dystrophy syndrome (RSDS) are changing. Although sympathetic influences are still viewed as the most likely mechanism underlying the development and/or perpetuation of RSDS, these influences are no longer ascribed to an increase in sympathetic tone. Rather, the most likely mechanism may be increased sensitivity to catecholamines due to sympathetic denervation with an increase in the number and/or sensitivity of peripheral axonal adrenoceptors. Several other pathophysiological mechanisms have been suggested, including neurogenic inflammation with the release of neuropeptides by primary nociceptive afferents and sympathetic efferents. These neuromediators, particularly substance P, calcitonin gene-related peptide, and neuropeptide Y (NPY), may play a pivotal role in the genesis of pain in RSDS.

Thao Pham^, and Pierre Lafforgue
Joint Bone Spine
Volume 70, Issue 1, 1 February 2003, Pages 12-17

sympathectomy on insulin receptors and insulin action in isolated rat adipocytes

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

HG Joost and SH Quentin

Volume 229, Issue 3, pp. 839-844, 06/01/1984
Copyright © 1984 by American Society for Pharmacology and Experimental Therapeutics

Effect of autonomic and adrenal manipulation on the serum insulin level

3. Journal of Tissue Research Vol. 4 (1) 83-88 (2004) Pilo, B. and Yadav, V.

Division of Neuroendocrinology, Department of Zoology, Faculty of Science, The Maharaja Sayajirao University of Baroda, Vadodara-390 002 India. Email: bonnypilo@satyam.net.in

Mammalian glucose homoeostasis is partially controlled by glucose sensor mechanisms in the pancreatic endocrine cells and partially through autonomic nerves. The influence of the autonomic nervous system on pancreatic insulin secretion has been studied in the present study. Vagal sectioning decreased serum insulin significantly compared to that of the sham operated rats which could be the reason for the resulting hyperglycaemic condition prevailed in these rats. Bilateral adrenalectomy and chemical sympathectomy singly increased insulin level to the same extent. Even, when vagotomy was performed together with adrenalectomy, insulin level declined but this decrease is not as significant as that in vagotomized rats. Similar result was obtained with rat treated for chemical sympathectomy and vagotomy together and this slight decrease in insulin level could favour marginal hyperglycaemia.

Vasoconstrictor responses to immersion of the hand in ice water in the sympathetically denervated forearm were abolished

Vasoconstrictor responses to immersion of the hand in ice water in the sympathetically denervated forearm were abolished; during the second minute of the cold pressor test, vascular resistance had increased by 48±20 percent in the innervated limb, whereas it had decreased by 17±5 percent in the denervated limb (P<0.02> limbs).

Figs. 1 and 2 show that L-NMMA infusion evoked a roughly 3-fold larger increase in vascular resistance in the denervated forearm than in the innervated calf. In the forearm, vascular resistance increased by 58±10 percent during L-NMMA infusion whereas in the calf, it increased only by 21±6 percent (P<0.001, forearm vs. calf). The L-NMMA induced vasoconstriction was reversed by L-arginine, but not by D-arginine, infusion (Table 1). In contrast to L-NMMA, infusion of an equipressive dose of phenylephrine increased the vascular resistance comparably in the denervated and the innervated limb (by 24±3 and 26±7 percent, respectively; P>0.5, forearm vs. calf).

Here we used subjects having undergone thoracic sympathectomy for hyperhydrosis, to probe the role of the peripheral sympathetic nervous system in the modulation of the vascular responsiveness to nitric oxide synthase inhibition. We found that sympathectomy markedly potentiated the vasoconstrictor effect of L-NMMA infusion. The L-NMMA induced vasoconstrictor effect was almost three times larger in the denervated than in the innervated limb. These findings provide the first evidence for an important interplay between the peripheral sympathetic nervous system and the L-arginine–nitric-oxide system in the regulation of the vascular tone in humans, and indicate that sympathetic innervation attenuates the vasoconstrictor effect of nitric oxide synthase inhibition.

Cardiovascular Research 1999 43(3):739-743; doi:10.1016/S0008-6363(99)00084-X
© 1999 by European Society of Cardiology

sympathectomy of peripheral nerves has been demonstrated to augment antibody response following immunization

Chemical sympathectomy of peripheral nerves has been demonstrated to augment antibody response following immunization with specific antigen.

Surgery: Basic Science and Clinical Evidence

By Jeffrey A. Norton, R. Randall Bollinger

Contributor Jeffrey A. Norton

Published by Springer, 2001