Decreased brain metabolism, rather than an increased intracranial pressure, is the cause of decreased cerebral blood flow after superior cervical sympathetic ganglionectomy

"The reduced brain metabolism and consequently reduced cerebral perfusion in the late 

postsympathectomy period could account for reduction in CSF production (Bering3)."

"In support of the above statement we mention that on the late postsympathectomy (11 to 24 months) group of dogs besides the lowered CBF 

(31.36 ml/100 gm brain weight/minute) and MCP (79.3 mm NS) also a lowered MVP (46.5 mm NS) was found. These data indicate that cervicalsympathectomy has a profound and intricate effect on the dynamics of cerebrovascular fluids and probably, in the background of all observedphenomena, a decreased cerebral metabolism as a sympathectomy effect is the underlying cause. Correspondingly the cerebral metabolic rate ofoxygen (CMR O2) decreased to 2.94 and 2.43 ml of O2/IOO gm brain weight/ minute in the sympathectomized groups." 

"Decreased brain metabolism, rather than an increased intracranial pressure, is the cause of decreased cerebral blood flow after superior 

cervical sympathetic ganglionectomy."

http://archsurg.ama-assn.org/cgi/content/summary/90/3/418

After the sympathectomy, the high night time excretion was clearly abolished

The amount of 6-sulphatoxymelatonin, the chief metabolite of melatonin, in the urine was measured in nine patients, who were subjected to bilateral sympathectomy at the second thoracic ganglionic level for treatment of hyperhidrosis of the palms. All patients showed before surgery a normal 6-sulphatoxymelatonin excretion with a peak in the excretion 
during the night time. After the sympathectomy, the high night time excretion was clearly abolished in five patients but remained high in four patients...
http://www.ncbi.nlm.nih.gov/pubmed/16647807

denervation on protein synthesis and degradation in adult rat diaphragm muscle

Previous studies showed that unilateral denervation (DNV) of the rat diaphragm muscle (DIAm) results in loss of myosin heavy chain protein by 1 day after DNV. We hypothesize that DNV decreases net protein balance as a result of activation of the ubiquitin-proteasome pathway. In DIAm strips, protein synthesis was measured by incorporation of ³H-Tyr, and protein degradation was measured by Tyr release at 1, 3, 5, 7, and 14 days after DNV. Total protein ubiquitination, caspase-3 expression/activity, and actin fragmentation were analyzed by Western analysis. We found that, at 3 days after DNV, protein synthesis increased by 77% relative to sham controls. Protein synthesis remained elevated at 5 (85%), 7 (53%), and 14 days (123%) after DNV. At 5 days after DNV, protein degradation increased by 43% relative to sham controls and remained elevated at 7 (49%) and 14 days (74%) after DNV. Thus, by 5 days after DNV, net protein balance decreased by 43% compared with sham controls and was decreased compared with sham at 7 (49%) and 14 days (72%) after DNV. Protein ubiquitination increased at 5 days after DNV and remained elevated. 

http://jap.physiology.org/content/107/2/438.full

fall in the resting membrane potential (RMP) that was identical to the effect of surgical denervation

ACh blockade using a-BuTx produced a fall in the resting membrane potential (RMP) that was identical to the effect of surgical denervation with respect to the time of onset, rate of development, and extent of change. Blockade of nerve impulses using TTX produced a similar but partial change in the RMP that began later and progressed more slowly than that of denervation. 

Similarly, the increase of extrajunctional ACh receptors following cY-BuTx-induced blockade of ACh transmission was identical to that of surgical denervation. By contrast, the effect of nerve 

impulse block using TTX was less pronounced at equivalent time points. 

Our findings indicate that specific pharmacological blockade of ACh transmission produces 

changes in the RMP and extrajunctional ACh receptors of skeletal muscle that are quantitatively equivalent to those of denervation. This suggests that ACh transmission itself mediates the nerve’s trophic regulation of these muscle properties. 

The Journal of Neuroscience,  Vol. 2, No. 2, pp. 232-243 . February 1982 

The denervation effect of smooth muscles in this instance is related to the delayed response of the smooth muscle

The denervation effect of smooth muscles in this instance is related to the delayed response of the smooth muscles and not the effect of denervation.The result, however, is the same and the four components of denervation (super-duration/delayed response, hyper-excitability, increased susceptibility and super-reactivity) are mimicked exactly by inelastic and inflexible smooth muscles. 

Autonomic nervous system: The autonomic nervous system of most fibromyalgia patients is imbalance with predominate excessive sympathetic outflows. The term dysautonomia is often used to describe these patients' S / S related to the ANS. There are significant problems related to smooth muscle dysfunctions (see effect of relaxin on smooth muscles) and the control of these organs as alluded to in the beginning of this discussion. This has to do with imbalance of the relatively increased sympathetic or decreased parasympathetic tone of the ANS. The inability of the ANS to maintain a homeostatic level of control on the smooth muscles and sphincters of many of the inner organs results in the under/ over performance of these organs. 

http://www.encognitive.com/node/12690

Surgical sympathectomy produces most of the retinal changes noted in the retina of an STZ-treated rat in a non-diabetic rat

Sympathectomy significantly increases gene and protein expression of iNOS, as well as levels of PGE2 and protein expression of PGE2-EP2 receptor subtype. Isoproterenol treatment for 6 h to human retinal endothelial cells grown in high glucose medium reduced iNOS protein expression, but had no effect on PGE2 levels or PGE2 receptor protein expression. iNOS expression was attenutated by stimulation with xamoterol, while BRL37344 had no effect, suggesting that the iNOS effects are mediated by beta1-adrenergic receptors. These results suggest that loss of sympathetic activity, as occurs in diabetes, results in an upregulation of iNOS and PGE2-EP2 receptor protein expression, as well as PGE2 levels. Isoproterenol stimulation of human retinal endothelial cells cultured in a hyperglycemic environment decreased iNOS expression with no change in PGE2 levels, suggesting that only iNOS expression is modulated by sympathetic neurotransmission in endothelial cells. Overall, these results further the idea that alterations in sympathetic neurotransmission may result in many of the changes noted in the retina of the STZ-treated rat.
http://www.ncbi.nlm.nih.gov/pubmed/17067575

CERVICAL SYMPATHECTOMY AND CEREBROSPINAL FLUID PRESSURE: THEIR RELATIONSHIP TO BRAIN METABOLISM

http://www.ncbi.nlm.nih.gov/pubmed/14247422

The effect of carotid ligation and cervical sympathectomy in guinea-pigs on the ascorbic acid content of the aqueous humour at varying plasma levels

http://www.ncbi.nlm.nih.gov/pubmed/12985402

Surgical Denervation of Ocular Sympathetic Afferents Decreases Local Transforming Growth Factor-β and Abolishes Immune Privilege

Mounting evidence points to a role for the sympathetic nervous system in suppressing inflammation. This role might be of specific relevance for immune privilege in the eye, where, sporadically, patients with denervated sympathetic fibers develop chronic inflammation.

Our results show that in the absence of functional sympathetic fibers, the eye loses its ability to prevent either the immune rejection of intraocular allogeneic tumor cells or the suppression of delayed type hypersensitivity responses against soluble antigens injected in the anterior chamber. This loss of immune privilege is accompanied by a decrease in the concentration of transforming growth factor-β in the aqueous humor. These results suggest that immune privilege is lost in the absence of a functional sympathetic innervation of the eye, allowing intraocular immune responses to become exaggerated. We conclude that ocular sympathetic nerves are critical for the generation and maintenance of immune privilege in the eye through the facilitation of local transforming growth factor-β production.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2731140/

Chest wall paresthesia affects a significant but previously overlooked proportion of patients following sympathectomy

Paresthetic discomfort distinguishable from wound pain was described by 17 patients (50.0%). The most common descriptions were of ‘bloating’ (41.2%), ‘pins and needles’(35.3%), or ‘numbness’ (23.5%) in the chest wall. The paresthesia resolved in less than two months in 12 patients (70.6%), but was still felt for over 12 months in three patients (17.6%). Post-operative paresthesia and pain did not impact on patient satisfaction with the surgery, whereas compensatoryhyperhidrosis in 24 patients (70.6%) did (P=0.001). The rates and characteristics of the paresthesia following needlescopic VATS are similar to those observed after conventional VATS. Conclusions: Chest wall paresthesia affects a significant but previously overlooked proportion of patients following needlescopic VATS.
Eur J Cardiothorac Surg 2005;27:313-319

Autonomic determinism: the modes of autonomic control, the doctrine of autonomic space, and the laws of autonomic constraint

Contemporary findings reveal that the multiple modes of autonomic control do not lie along a single continuum extending from parasympathetic to sympathetic dominance but rather distribute within a 2-dimensional space. The physiological origins and empirical documentation for the multiple modes of autonomic control are considered. Then a formal 2-dimensional conception of autonomic space is proposed, and a quantitative model for its translation into a functional output surface is derived. It is shown that this model (a) accounts for much of the error variance that has traditionally plagued psychophysiological studies, (b) subsumes psychophysiological principles such as the law of initial values, (c) gives rise to formal laws of autonomic constraint, and (d) has fundamental implications for the direction and interpretation of a wide array of psychophysiological studies.
http://www.ncbi.nlm.nih.gov/pubmed/1660159?dopt=Abstract

Chemical sympathectomy impairs bone resorption in rats: a role for the sympathetic system on bone metabolism

http://www.ncbi.nlm.nih.gov/pubmed/10574574?dopt=Abstract

Neuroendocrine regulation of autoimmune/inflammatory disease

http://www.ncbi.nlm.nih.gov/pubmed/11375112?dopt=Abstract

Predisposing factors to RSD include trauma, peripheral nerve injury

Emergency orthopedics: the extremities - Google Books Result

Robert Rutha Simon, Steven J. Koenigsknecht - 2001

yet, sympathectomy (surgical trauma/injury) to the sympathetic chain and nervous system is used as a 'cure' for this condition. Systematic reviews failed to support the effectiveness of sympathectomy in the treatment of this condition, yet it remains embedded in medical practice.

sympathectomy may result in the loss of a trophic influence which is important in the regulation of osteogenesis

Grain counts over periosteal osteoblasts of the femoral diaphysis and osteoblasts mesial to the first molar in the mandible demonstrated a significantly reduced uptake of ³H-proline in the sympathectomized rats. The data provide direct evidence of sympathetic influence on osteoblastic activity and suggest that sympathectomy may result in the loss of a trophic influence which is important in the regulation of osteogenesis.

Cell and Tissue Research

Volume 216, Number 1, 215-220, DOI: 10.1007/BF00234556

Progressive facial hemiatrophy following cervical sympathectomy

Unilateral cervical sympathectomy of the month-old rat produced a condition simulating progressive facial hemiatrophy during a postoperative period of 2–4 months. While the gross extent of the lesion produced varied, the histological appearance was uniform; adipose tissue alone was diminished. Osseous, muscular and vascular structures of the facial skull appeared unaltered under these experimental conditions. No evidence of a neurotrophic influence on either the growth or maintenance of bone form was found. The mechanism of production of the adipose atrophy remains unknown.
Archives of Oral Biology
Volume 1, Issue 3, January 1960, Pages 254-258, IN11-IN14 

defects in cartilage after sympathectomy

Profound degenerative changes occur in skeletal muscle following interruption of it's nerve supply and it has therefore been quite reasonably concluded that the motor nerves exert a definite trophic influence over striated muscle (Tower, 1939). However in the case of bone innervation, one is dealing with a quite different phenomenon.

Influence of the nervous system on bone and joints

1. Kendall B. Corbin,
2. Joseph C. Hinsey

Article first published online: 3 FEB 2005

The ANS provides physiological stability

The autonomic nervous system dynamically controls the response of the body to a range of external and internal stimuli, providing physiological stability in the individual. With the progress of information technology, it is now possible to explore the functioning of this system reliably and non-invasively using comprehensive and functional analysis of heart rate variability. This method is already an established tool in cardiology research, and is increasingly being used for a range of clinical applications. This review describes the theoretical basis and practical applications for this emerging technique.

Functional assessment of heart rate variability: physiological basis and practical applications .

International Journal of Cardiology , Volume 84 , Issue 1 , Page 1

J . Pumprla

Copyright © 2003 Elsevier Inc

Autonomic dysequilibrium (local sympathectomy) leading to obesity

A similar reduction of fat mobilization from fat depots occurs after VMH lesions, as after local sympathectomy, suggesting that the sympathetic pathway to the adipose tissue runs through the VMH.
Bray and York hypothesize that the change in energy balance in animals after VMH lesions is a result of autonomic dysequilibrium. The sympathetic outflow is reduced and the parasympathetic outflow increased. This shift in balance results in hyperinsulinemia and altered metabolic pathways leading to obesity. During the digestion and metabolism of a meal, the autonomic nervous system provides important (but not sole) feedback control on satiety.

The Nervous System and Adipose Tissue, By Katharine Dalziel, MD, MBBS, MRCP
Clinics in Dermatology
October-December 1989, Volume 7, Number 4, pages 62-77

abnormal sympathetic activity may cause pain following sympathectomy

Further evidence suggesting that abnormal sympathetic activity may cause pain comes from reports of pain following sympathectomy. This has occurred after stellate ganglion block and lumbar sympathectomy.
The Nervous System and Adipose Tissue, By Katharine Dalziel, MD, MBBS, MRCP
Clinics in Dermatology
October-December 1989, Volume 7, Number 4, pages 62-77

Neuroma formation at the ends of the sympathetic chain after Sympathectomy

The authors conclude recomemnding the application of clips and if the syndrome nevertheless appears novocaine infiltration of the upper end of the sympathetic chain. The authors are convinced that the theory of Hermann and Cooley about neuroma formation at the ends of the sympathetic chain after resection of a segment is true.
http://www.revangiol.com/sec/resumen.php?or=web&i=e&id=227082.

Traumatic neuroma follows different forms of nerve injury (often as a result of surgery). They occur at the end of injured nerve fibres as a form of ineffective, unregulated nerve regeneration; it occurs most commonly near a scar, either superficially (skin, subcutaneous fat) or deep (e.g., after a cholecystectomy). They are often very painful. It is also known as "pseudoneuroma".

Post-sympathectomy neuralgia is a complex neuropathic and central deafferentation/reafferentation syndrome

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.

Pain. 1996 Jan;64(1):1-9
http://www.ncbi.nlm.nih.gov/pubmed/8867242?ordinalpos=2&itool=EntrezSystem2.PEntrez.Pubmed.Pubmed_ResultsPanel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum

sensory abnormalities, abnormal body sweating, and pathologic gustatory sweating after sympathectomy

The aim of this study is to describe the incidence and characteristics of pain, sensory abnormalities, abnormal body sweating, and pathologic gustatory sweating in pain patients with persistent post-sympathectomy pain.
Results: Seventeen adults (13 females and 4 males) with a mean age of 37 years (range 25-52) at the time of sympathectomy met the inclusion criteria. Five of the 17 patients experienced temporary pain relief for an average of 4 months (range 2-12 months), 3/17 retained the same pain as before the surgery, 1 patient was cured of her original pain but experienced a new debilitating pain, and 8/17 patients continued to have the same or worse pain in addition to a new or expanded pain. Pathologic gustatory sweating was present in 7/11 patients asked, and abnormal sweating (known as compensatory hyperhidrosis) in 11/13 patients asked. Discussion: The present study does not allow for conclusions about the effectiveness of surgical sympathectomy for neuropathic pain.
However, our findings indicate that if the pain persists after the procedure, the complications may be quite serious and at times worse than the problem for which the surgery was originally performed.
The Clinical journal of pain
2003, vol. 19, n^o3, pp. 192-199
http://cat.inist.fr/?aModele=afficheN&cpsidt=14775091

Effect of local autonomic denervation on in vitro responsiveness of lymphocytes

The results further indicate that an appropriate sympathetic and parasympathetic local environment may be needed for immunomodulation, as well as for cyclosporine activity in lymphoid tissue.
Journal of the Autonomic Nervous System
Volume 62, Issue 3, 17 February 1997, Pages 155-162
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6T05-3PKTG6C-6&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=da81efda6c250763623b89537aed8109

"Sympathectomy is a technique about which we have limited knowledge, applied to disorders about which we have little understanding."

http://www.pfizer.no/templates/Page____886.aspx

POSTSYMPATHECTOMY PAIN AND CHANGES IN SENSORY NEUROPEPTIDES

Postsympathectomy limb pain, postsympathectomy parotid pain, and Raeder's paratrigeminal syndrome are pain states associated with the loss of sympathetic fibres and in particular with postganglionic sympathetic lesions. There is a characteristic interval of about 10 days between surgical sympathectomy and onset of pain. It is proposed that this pain in man is correlated with the delayed rise in sensory neuropeptides seen in rodents after sympathectomy. These chemical changes probably reflect the sprouting of sensory fibres and may result from the greater availability of nerve growth factor after sympathectomy. The balance between the sensory and sympathetic innervations of a peripheral organ may be determined by competition for a limited supply of nerve growth factor.
The Lancet, Volume 326, Issue 8465, Pages 1158 - 1160, 23 November 1985

Following sympathectomy the basal t-PA activity in plasma was 70% less than controls

Following sympathectomy: (i) the basal t-PA activity in plasma was 70% less than controls (2.92 ± 1.96 versus 9.33 ± 1.72 IU/ml;P ≤ 0.001); (ii) the acute release from isolated vessels induced by bradykinin or phenylephrine was comparably reduced; and (iii) the greatest reductions occurred in densely innervated small vessel explants. The results provide new support for an autonomic regulation of neural t-PA release into the vessel wall matrix and blood of densely innervated thin-walled microvessels.

Blood Coagulation & Fibrinolysis:

September 2002 - Volume 13 - Issue 6 - pp 471-481

link between sympathectomy and osteoclast-mediated bone resorption

Recent investigations have demonstrated a link between sympathectomy and osteoclast-mediated bone resorption. The exact nature of this link, however, is unknown, We hypothesize that substance P, a potent vasoconstrictive neuropeptide found in peripheral sensory fibers, including those innervating bone, is the mediator of this phenomenon. To test this theory, the effects of substance P on in vitro calcium release from cultured neonatal mouse calvaria were assessed. In addition, an in vivo study was conducted whereby gerbils were injected with capsaicin to eliminate substance P-containing fibers before sympathectomy with 6-hydroxydopamine. If the effects of 6-hydroxydopamine were eliminated by prior administration of capsaicin, the role of sensory nerves in sympathectomy-induced resorption would be strongly implicated.


The results indicate that substance P is capable of inducing resorption and that substance P-containing sensory nerves are required for the induction of resorption after sympathectomy in the gerbil.

Otolaryngol Head Neck Surg November 1, 1995 vol. 113 no. 5 569-581

diabetic autonomic neuropathy is due to a lesion of the sympathetic nerve supply to the skin

"We conclude that the diabetic anhidrotic syndrome, a form of diabetic autonomic neuropathy, is due to a lesion of the sympathetic nerve supply to the skin."

Diabetologia

Volume 22, Number 2, 96-99, DOI: 10.1007/BF00254836

Sympathectomy IS a (surgically caused) lesion of the sympathetic nerve supply to the skin (and other structures)

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

Regulation of peripheral inflammation

It is clear that the spinal adenosine effect requires intact somatic connectivity. Information on pain and inflammation in the periphery is transmitted to the nervous system, where increased spinal adenosine levels can suppress peripheral inflammation.
Experimental Neurology
Volume 184, Issue 1, November 2003, Pages 162-168

Sypathetic nervous system (SNS) modulation of immunity

Sypathetic nervous system (SNS) modulation of immunity. The role of the sympathetic nervous system in regulation of immunity is examined in mice that are chemically-denervated by injection of the neurotoxin 6-hydroxydopamine (6-OHDA). This results in a strain-dependant elevation of Th1 and Th2 cytokines and antibody titers. Denervation also results in a robust, but transient, expression of central Fos protein and corticotrophin releasing hormone, as well as an elevation in corticosterone levels in denervated mice. The interrelationships of this HPA axis activation, loss of peripheral sympathetics, and altered immune function is being explored.

Jan A. Moynihan
Associate Professor of Psychiatry, Microbiology and Immunology and of Oncology

Rice PA, Boehm GW, Moynihan JA, Bellinger DL, Stevens SY. Chemical sympathectomy alters numbers of splenic and peritoneal leukocytes. Brain Behav Immun. 16:62-73, 2002.

Rice PA, Boehm GW, Moynihan JA, Bellinger DL, Stevens SY. Chemical sympathectomy increases the innate immune response and decreases the specific immune response in the spleen to infection with Listeria monocytogenes. J Neuroimmunol 114:19-27, 2001.