contributing to the elevated susceptibility to ventricular fibrillation

contributing to the elevated susceptibility to ventricular fibrillation

Sympathetic denervation is frequently observed in heart disease. To investigate the linkage of sympathetic denervation and cardiac arrhythmia, we developed a rat model of chemical sympathectomy by subcutaneous injections of 6-hydroxydopamine (6-OHDA).
We observed that sympathectomy (i) decreased cardiac sympathetic nerve density and norepinephrine level, (ii) reduced the protein expression of Kv4.2, Kv1.4, and Kv channel-interacting protein 2 (KChIP2), (iii) decreased current densities and delayed activation of I_to channels, (iv) reduced the phosphorylation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) and cAMP response element-binding protein (CREB), and (v) increased the severity of ventricular fibrillation induced by rapid pacing.
We conclude that chemical sympathectomy downregulates the expression of selective Kv channel subunits and decreases myocardial I_to channel activities, contributing to the elevated susceptibility to ventricular fibrillation.
Can. J. Physiol. Pharmacol. 86(10): 700–709 (2008)

Sterility following lumbar sympathectomy

Bacq (1931) found that bilateral lumbar sympathectomy in rabbits resulted in sterility with prolonged copulation and absence of orgasm.
J. Reprod. Fertil. (1964) 7, 113-122

Altered Cerebral Blood Flow following Sympathectomy

The subject has recently been studied by James, Millar&Purves who measured the cerebral vascular response to hypoxia with all nerves intact and following division or stimulation of the vagus and cervical sympathetic nerves. The effect of sympathectomy (...) is seen to consist of an elevation of both grey and white matter blood flow 40-50 per cent above control over the range of PaO2 tested, 35 to 440 mmHg. When the cervical sympathetic nerve as stimulated at constant frequency and intensity, cortical flow was reduced to control levels.

The Physiology of the Cerebral Circulation (Monographs of the Physiological Society) by M. J. Purves (Hardcover - May 31, 1972)

decrease in resting pulmonary resistance that follows thoracic thoracic sympathectomy

Diminished sympathetic constrictor discharge to pulmonary arterioles probably contributes to the lowering of resistance. No direct evidence for such an action has been presented, but the decrease in resting pulmonary resistance that follows thoracic thoracic sympathectomy shows that the potential for such a response exists. Whatever the mechanism, the net result is that pulmonary blood flow can be increased greatly without raising intravascular pressures to a degree that would encourage capillary transudation of fluid.

Cardiovascular physiology

By William R. Milnor

New York : Oxford University Press, 1990.

Sympathetic nervous system control of anti-influenza CD8+ T cell responses

Adoptive transfer experiments indicate that enhanced CD8⁺ responses do not result from permanent alterations in CD8⁺ T cell function in sympathectomized mice. Rather, additional findings suggest that the sympathetic nervous system tempers the capacity of antigen-presenting cells to activate naïve CD8⁺ T cells. We also show that antiviral CD8⁺ T cell responses are enhanced by administration of a β₂ (but not β₁ or α) adrenergic antagonist. These findings demonstrate a critical role for the sympathetic nervous system in limiting CD8⁺ T cell responses and indicate that CD8⁺ T cell responses may be altered in patients using β-blockers, one of the most widely prescribed classes of drugs.
PNAS March 31, 2009 vol. 106 no. 13

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

In another work on dogs, sympathectomy caused a state similar to atrophic rhinitis in man

Relationship Between the Vegetative Innervation and the Sensibility of the Nasal Mucosa
Z. Krajina; Z. Poljak
Acta Oto-Laryngologica, 1651-2251, Volume 79, Issue 3, 1975, Pages 172 – 175

Structural changes associated with parotid "degeneration secretion" after post-ganglionic sympathectomy

This loss of granules is considered to be due to sympathetic "degeneration secretion" caused by the release of noradrenaline from the degenerating adrenergic nerves between 12 and 24 hours after ganglionectomy. This is thought to be the first example of morphological change resulting from "degeneration activation" to be recorded microscopically.
Cell Tissue Res. 1975 Sep 16;162(1):1-12.

PMID: 1175216 [PubMed - indexed for MEDLINE]

Gray Hair and Sympathectomy: Report of a Case

LERNER
Arch Dermatol.1966; 93: 235-236.

acinar degranulation following sympathectomy

Chronic bilateral postganglionic sympathectomy (4-6 weeks duration) caused a drastic reduction in the capacity of the gland to secrete saliva in response to parasympathetic stimulation, reaching only one-third of that from normal animals. The initial output of amylase was greater than in normal animals but the total output was similar. The control unstimulated sympathectomized glands appeared similar morphologically to normal resting glands. However, on the parasympathetically stimulated side, besides the usual amount of acinar degranulation, there was also a conspicuous development of acinar vacuolation, not seen in the other groups of animals.
J. Physiol. November 15, 2008 586:5537-5547

Cervical sympathectomy inhibits axonal transport of gonadotropin-releasing hormone

To examine the effects of cervical sympathectomy on the transport of gonadotropin-releasing hormone (GnRH) between the hypothalamic neurons and the median eminence, 16 male rats were assigned into four groups: control (C), light (L), light-sympathectomy (LS), and light-colchicine (LC).

Considering the action of colchicine, which inhibits axonal transport, it is suggested that cervical sympathectomy also inhibits axonal transports of GnRH between the GnRH neurons and the median eminence during continuous exposure to light.
Journal of Anesthesia
Volume 10, Number 3 / September, 1996

Calcitonin gene-related peptide and substance P contribute to reduced blood pressure in sympathectomized rats

Am J Physiol Heart Circ Physiol 289: H1169-H1175, 2005.

Sympathectomized rats displayed reductions in blood pressure (BP) and atria norepinephrine levels, whereas NGF levels in the DRG, spleen, and ventricles were increased. Sympathectomy also enhanced CGRP and SP mRNA and peptide content in DRG. Administration of CGRP and SP receptor antagonists increased the BP in sympathectomized rats but not in the controls. Thus sympathectomy enhances sensory neuron CGRP and SP expression that contributes to the BP reduction.

Neurogenic and non-neurogenic inflammation in the rat paw following chemical sympathectomy

http://www.ncbi.nlm.nih.gov/pubmed/1723182?dopt=Abstract

Neuroscience. 1991;45(3):761-5.
Neonatal guanethidine sympathectomy caused an 86% depletion of noradrenaline in the paw skin and neurogenic plasma protein extravasation upon antidromic nerve stimulation was impaired. Sensory neuropeptides were unchanged in the skin after neonatal guanethidine and only calcitonin gene-related peptide content was increased in the spinal cord and sciatic nerves. The other observations (i.e. the sensitivity towards heat stimuli, the neurogenic mustard oil inflammation and the non-neurogenic carrageenan oedema) were similar to those observed after neonatal 6-hydroxydopamine treatment.

Sympathectomy exaggerates antihypertensive effect of vasopressin withdrawal

The results are consistent with the hypothesis that withdrawal of sympathetic activity is a contributing factor or a prerequisite condition for development of a WAP.(withdrawal-induced antihypertensive phenomenon)
AJP - Heart and Circulatory Physiology, Vol 268, Issue 1 1-H6, Copyright © 1995 by American Physiological Society

plasma levels of natriuretic peptides in response to sympathectomy

The occurrence of receptor binding sites for natriuretic peptides was examined by in vitro receptor autoradiography. In contrast to the marked occurrence of natriuretic peptide receptor binding sites seen in the ventricular endocardium of control rats, the sympathectomized rats exhibited a decreased number of binding sites for natriuretic peptides in the endocardium of both the right and left chambers. Interestingly, this was found in parallel with a significant decrease of systolic and diastolic blood pressure and increased plasma levels of pro-atrial natriuretic peptide in the treated group of rats. These findings, together with those in previous studies, give support to an idea that one part of the blood pressure-decreasing effects, seen in patients treated with β-adrenergic blockade, might be through a reduction of the natriuretic clearance receptor C, then giving rise to increased levels of atrial natriuretic peptide.

http://cat.inist.fr/?aModele=afficheN&cpsidt=17030448

Abolition of sympathetic skin responses following endoscopic thoracic sympathectomy

The recording of sympathetic skin responses (SSRs) is a simple, electrophysiological method to assess sympathetic nerve function. Within the last 10 years, SSRs have mainly been applied to delineate peripheral and central nervous system diseases, although the sympathetic nature of these responses was not fully documented, e.g., by a study of sympathectomy. We therefore recorded SSRs before and after 30 cases of endoscopic thoracic sympathectomy. The main indication was palmar hyperhidrosis, in which we found two types of SSR abnormalities. Most patients exhibited normal SSR waveforms but with increased amplitudes. The other patients exhibited abnormal SSRs which did not occur as single responses but as several consecutive waves.

Muscle & Nerve

Volume 19 Issue 5, Pages 581 - 586

Published Online: 7 Dec 1998

cervical sympathectomy resulted in a rapid degeneration in some of the cells in the sinuatrial and atrioventricular nodes

This study describes the ultrastructural changes in the sinuatrial and atrioventricular nodes of the heart of the monkey (Macaca fascicularis) after right cervical sympathectomy. Obvious changes in the nodal cells were seen one day after operation. Numerous glycogen particles grouped together to form electron-dense patches containing vacuoles in the cytoplasm. At three days after operation, intracellular organelles exhibited fragmentation and dissolution. By five and seven days after operation, the affected cells were vacuolated and some were swollen and appeared to have degenerated. Simultaneously, there was massive infiltration of macrophages were present nodal tissues. Axon profiles and terminals showing various degrees of degeneration were present in the vicinity of the nodal cells throughout the period of study.

J Anat. 1984 October; 139(Pt 3): 449–461.

Electrophysiology - effect on the heart

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

Cardiovascular Research 1982 16(9):524-529; doi:10.1093/cvr/16.9.524

Infra-stellate upper thoracic sympathectomy results in a relative bradycardia during exercise, irrespective of the operated side

Patients should be informed of the exercise bradycardia resulting from ISS.

Eur J Cardiothorac Surg 2001;20:1095-1100

Sympathectomy induces adrenergic excitability of cutaneous C-fiber nociceptors

Journal of Neurophysiology, Vol 75, Issue 1 514-517, Copyright © 1996 by APS

The induction of adrenergic excitability in CPMs by sympathectomy is suggested to be a counterpart to postsympathectomy neuralgia in human beings and a possible part of the mechanism leading to sympathetically related pain states.

The results provide new evidence about the change in atrial natriuretic peptide levels that occurs when sympathetic innervation is altered.

PMID: 9799658 [PubMed - indexed for MEDLINE]

J Mol Cell Cardiol. 1998 Oct;30(10):2047-57.

Neuroma following nerve injury/surgery

When a nerve is cut, the piece of nerve that is beyond the cut point eventually dies, however, its Schwann cells, the cells that encircle the nerve fibers remain for a much longer time. These Schwann cells secrete a chemical messenger known as nerve growth factor that tells the cut end of nerve where to grow back. So the cut end of nerve will send out multiple sprouts in the direction of the nerve growth factor, however, these sprouts do not go out in an orderly manner, instead they grow out in all directions and eventually cluster and form a knot of nerve fibers. This eventually leads to the formation of a TRUE neuroma or a END BULB or STUMP neuroma.

www.tarsaltunnelcenter.com/assets/recurrent.shtml

Risks during Thoracic Sympathectomy - Surgery not as safe as reported

T(2)-T(3) ganglionectomy significantly decreases pulse rate and systolic blood pressure, reduces myocardial oxygen demand, increases left ventricular ejection fraction and prolongs Q-T interval. A certain loss of lung volume and decrease of pulmonary diffusion capacity for CO result from sympathectomy. Histomorphological muscle changes and neuro-histochemical and biochemical effects have also been observed.

http://www.ncbi.nlm.nih.gov/pubmed/14673672

 

a significant impairment of the heart rate to workload relationship was consistently observed following sympathectomy

Several reports also demonstrate significantly lower heart rate increases during exercise in subjects who have undergone bilateral ISS [9–12] compared to pre-surgical levels. In spite of this high occurrence, recent reviews on the usual collateral effects of thoracic sympathectomy still do not include these possible cardiac consequences [6].
The aim of the present prospective study was to confirm that a significant impairment of the heart rate to workload relationship was consistently observed following unilateral and/or bilateral surgery.
Eur J Cardiothorac Surg 2001;20:1095-1100
http://ejcts.ctsnetjourna...i/content/full/20/6/1095

 

disturbed peripheral vascular and heart rate responses after sympathectomy

Thoracic sympathectomy can result in reduced sweating and disturbed peripheral vascular and heart rate responses. Patients should be warned that these mechanisms may play a role in the development of exertional heat stroke.

Alan D.L. Sihoe, FRCSEd(CTh)^a,_*, Raymond W.T. Liu, MRCP^b, Alex K.L. Lee, MRCP^b, Chak-Wah Lam, FHKAM^b, Lik-Cheung Cheng, FRCS

 

Even epidural blockade limited only to the thoracic dermatomes is liable to cause complete sympathectomy, including cardiac sympathetic denervation. The ensuing vasodilation and bradycardia lead to hypotension, poor tolerance of mechanical interference with the heart, and inability to respond to acute changes in intravascular volume or body position. This symptom complex is especially troublesome to manage during intrathoracic operations when avoidance of hypervolemia is emphasized.

Thoracic sympathectomy has two other potenital consequences: effect on bronchomotor tone and effect on oxygenation.

During intrathoracic procedures using one-lung ventilation, a right-to-left intrapulmonary shunt is intentionally created (in the form of the nonventilated lung). The ensuing arterial oxygen tension (PaO2) is determined by a complex interaction involving cardiac output, mixed venous oxygen tension, the status of the ventilated lung, size of the shunt, and most significantly, hypoxic pulmonary vasoconstriction (HPV).
HPV diverts pulmonary blood flow away from the shunt by vavsoconstriction in the nonventilated lung, and is the principal adaptive defense mechanism against arterial hypoxemia during one-lung ventilation. The cellular mechanism and regulation of HPV, and the possible role of the autonomic nervous system are not completely understood.
The effect of thoracic sympathectomy of HPV is even less well understood. Since potent vasodilators such as nitroprusside antagonize HPV-induced vasoconstriction and lower the arterial oxygen tension, it is reasonable to assume that HPV will become less effective with thoracic sympathectomy.
Clinical studies have produced conflicting conclusions, most probably because direct measurement of HPV is not possible in human studies, and the surrogate endpoing examined PaO2 is determined not only by HPV, but also by a host of interacting factors, some of which may be affected by the sympathectomy and can not be held constant.

Risk Factor for Neuraxial Anesthesia-Associated Bradycardia:
Block height higher than T5
Younger age

Spinal and Epidural Anesthesia By Cynthia Wong

Publication Date: 2007-01-01 Publisher: MCGRAW-HILL EDUCATION - EUROPE Country of origin: UNITED STATES

After thoracoscopic sympathectomy for hyperhidrosis, very severe discomfort and hyperhidrosis in the neighboring non-sympathectomized regions occurred with alarming frequency and intensity. (p.879)

Alteration in Cerebral Blood Flow after sympathectomy

Jeng and associates observed an increase in cerebral blood flow after T2 sympathectomy, and they suggested the possibility of using such a surgical approach to improve cerebral blood flow in patients with cerebral vascular insufficiency.

Youmans Neurological Surgery, 5th Edition
Publisher: Saunders
Publication Date: 2003-10-10

Sympathetic nerves protect against blood-brain barrier disruption

 http://www.ncbi.nlm.nih.gov/pubmed/7064183?holding=ukpmc

Effect of adrenalectomy or sympathectomy on spinal cord blood flow

After sympathectomy, RSCBF (regional spinal cord blood flow) was unchanged during hypothermia. In the cauda equina, flow fell in all hypothermic rats. The hypothermia-associated increases in RSCBF were not related to changes in mean arterial blood pressure. We conclude that adrenalectomy near-totally ablates the hypothermia-associated increase in RSCBF measured in intact rats and that abdominal sympathectomy totally ablates it. This evidence complements morphological evidence for adrenergic innervation of the spinal cord vasculature.Am J Physiol. 1991 Mar;260(3 Pt 2):H827-31. 

Ultrastructural changes in the nerves innervating the cerebral artery after sympathectomy
http://www.ncbi.nlm.nih.gov/pubmed/5498231?holding=ukpmc

The angina-relieving effects of sympathetic blockade

In the 1930's it was recognised by neurosurgeons performing destructive sympathectomies for angina pectoris that local anaesthetic infiltration around the stellate ganglion often resulted in pain relief outlasting the duration of action of the local anaesthetic drug^13. This observation has been more recently confirmed¹⁴, and is currently (June 1999) the subject of a large scale randomised double-blind placebo-controlled trial funded by the British Heart Foundation.

The pathogenesis of angina and myocardial infarction pain involves the activation of the afferent sympathetic pathway. A frequent and important consequence of pain (especially when severe) is the `flight or fight' response through activation of sympathetic efferents. The clinical image of the patient with an acute myocardial infarction (cold, clammy, sweaty, anxious, tachycardic) is secondary to this adrenergic activation. Therefore, angina might be regarded as the sensory component of a positive feedback loop, which cannot under these circumstances be conceived as resulting in benefit, and which may be considered to be a maladaption.

The angina-relieving effects of sympathetic blockade might be due to interference with this maladaptive feedback loop, in a similar manner to the way in which adenosine interrupts a re-entrant tachycardia. If such a loop exists, it may partly explain chronic refractory angina and the fact that temporary interruption of this pathway has a prolonged effect on pain¹⁴. Beneficial amelioration of angina can be achieved with repeated blocks¹⁴. There does not appear to be any predictability in the length of time a patient remains pain-free after successive blocks.

http://www.angina.org/source/pro/symp_block.htm

pain states associated with the loss of sympathetic fibres

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.
Lancet. 1985 Nov 23;2(8465):1158-60. 

Behavioral changes after sympathectomy

Six experiments are reported on the effects of 2,4,5-trihydroxyphenylethyl-amine (6-hydroxydopamine) on two-way escape and avoidance learning. Rats were tested on either escape or avoidance learning at 80 days of age after chemical sympathectomy at birth or 40 or 80 days of age. Neonatal and chronic sympathectomy (at 40 days), but not acute sympathectomy (at 80 days), resulted in depressed escape learning. Avoidance learning was affected by neonatal sympathectomy and partially by acute sympathectomy. The results have implications for the role of the autonomic nervous system in escape-avoidance learning.
J Comp Physiol Psychol 1976; 90:303-16.

normal forearm vasodilator response to mental stress was absent months or years after surgical sympathectomy

Additional indirect evidence on this topic in humans comes from a study conducted in the 1950s (3). In this study, the normal forearm vasodilator response to mental stress was absent months or years after surgical sympathectomy.
J Appl PhysiolVol. 92, Issue 5, 2019-2025, May 2002

Haematological changes during stress abolished by sympathectomy

To study haematological effects of emotional stress, blood samples were obtained from 29 healthy, normotensive, non-smoking males aged 20–34 years before, during and after 10 min of mental arithmetic. There were significant increases in pheripheral blood cell count, haemoglobin concentration, and haematocrit in response to mental stress. Parallel to these changes significant increases in heart rate, and systolic and diastolic blood pressure were observed. The relative increments of leucocyte (8%) and platelet (3·5%) count were significantly higher than the increase in haemoglobin concentration (2%). There was a significant positive correlation between the blood pressure increase and the mobilization of leucocytes, whereas the increase in erythrocyte count, haemoglobin concentration, and haematocrit showed significant positive correlations with heart rate reactivity. It is concluded that mental stress causes an increase in leucocyte and platelet count that could not solely be accounted for by the concurrent haemoconcentration.

The emotional leucocytosis observed in dogs has been claimed to be neurogenic in origin, since sympathectomy abolished the rise in leucocyte count (Garrey & Bryan, 19 3 5).
http://www3.interscience.wiley.com/journal/120731423/abstract 

sympathectomy can impair the autonomic nervous system’s increase of the heart rate in response to exercise

it has been shown that thoracic sympathectomy can impair the autonomic nervous system’s increase of the heart rate in response to exercise [6]. Although absolute tachycardia is not eliminated, given the endocrine and paracrine stimuli during exercise, the maximum heart rate reached during exercise has been shown to be significantly reduced after sympathectomy. Thus for a given workload during exercise, there will be a relative bradycardia. This may possibly affect the circulatory system’s ability to convey heat from the body core to the extremities for heat loss.
http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025 

thoracic sympathectomy has been demonstrated to abolish or alter sympathetic vasoconstrictive responses in the skin, and this may contribute to abnormal peripheral vascular responses to temperature [4]. Paradoxically it has been suggested that in some cases there may be abnormal vasoconstriction rather than the expected vasodilatation after sympathectomy [5]. It is not impossible that such atypical peripheral vascular responses to rising body temperature may have contributed to impaired heat loss during exercise or to an inappropriate response to shock on the development of the heat stroke.
http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025 

the abolition of sweating from the upper body as well as the axillae and both upper limbs may have significantly reduced the capacity of the patient to lose heat through sweating during exercise. Anhidrosis in the head and neck after sympathectomy affects a proportion of patients, but is often neglected in most reports of post-sympathectomy complications [3]. The loss of head and neck sweating in this patient may have further impaired overall heat loss. However we would also note that the degree of heat loss impairment after sympathectomy has never been quantified, and its effect on body temperature during exercise remains to be established.
http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025

"Although thoracic sympathectomy is commonly used to reduce upper limb sweating, it may also lead to facial anhidrosis and disturbed cardiovascular responses to temperature. The resultant effect on overall body heat loss has not been documented. We present a case of a young patient with previous thoracic sympathectomy who suffered severe heat stroke after heavy exercise.

An already impaired cardiovascular system is recognized to be a significant risk factor for development of heat stroke. In the post-sympathectomy patient, the abnormal sympathetic skin response may lead to peripheral vascular failure or the reduced cardiac chronotropic response may impair the body’s capacity to compensate for shock. These may have contributed to the rapid development of shock and severe multiple organ dysfunction syndrome in this patient.
He had multiple organ dysfunction syndrome develop, with severe renal and hepatic failure, grade II hepatic encephalopathy, and disseminated intravascular coagulation. He responded remarkably well to aggressive supportive measures including forced alkaline diuresis, and he was eventually discharged home after 1 month. The patient was previously a healthy, physically fit, nonsmoker. He worked as a body building trainer and led an active, sporty lifestyle. The only significant medical history was that he had received thoracic sympathectomy for axillary hyperhidrosis 4 years ago at another hospital.

http://ats.ctsnetjournals.org/cgi/content/full/84/3/1025

Glycogen accumulation in Reissner's membrane following chemical sympathectomy

Acta Otolaryngol. 1978 Nov-Dec;86(5-6):314-30.
PMID: 213930 [PubMed - indexed for MEDLINE]

Role of the ANS in cerebral circulation

It is proposed that the autonomic innervation of brain vessels participates in the control not only of the cerebral circulation but also of associated intracranial pressure phenomena.
Blood Vessels 1974;11:2-31

Sympathectomy alters cranial nerves and cerebral blood flow

Moya-Moya Syndrome

Moya Moya syndrome is a vasculopathy of the cranial arteries, usually the carotids, leading to progressive intracranial occlusion with distal collateral vessels. This is a very frequent cause of pediatric stroke in India(10,11). Children usually present with an acute focal deficit such as hemiplegia, whereas in later years sub-arachnoid hemorrhage is a common presenta-tion. Due to bilateral carotid involvement sometimes alternating hemiplegia is seen. The outcome varies widely without treatment. Moya Moya disease is usually idiopathic, although same radiographic pattern is seen in some patients with sickle cell disease, neuro-fibromatosis, postcranial irradiation and in various other conditions(15). There is no proven treatment of Moya Moya disease. Medical management involves use of aspirin but needs further testing. Surgical treatment involves cervical sympathectomy, intracranial graft of omentum or temporalis muscle and bypass of superficial temporal artery to the middle cerebral artery(34).

http://indianpediatrics.net/feb2000/personal.htm

sympathectomy greatly reduces ventilation

In conscious animals, cervical sympathectomy greatly reduces ventilation in normoxia and slightly affects ventilatory responses to hypoxia and hypercapnia, also suggesting an important role for these nerves in the control of breathing.
Eur Respir J 1998; 12: 177–184

reduces the amount of adrenaline

Cervical sympathectomy
A form of surgery that is useful for some people with LQTS. It reduces the amount of adrenaline and its by-products produced and delivered to the heart by certain nerves (the left cervical ganglia). It involves operating on the left neck and removing or blocking these nerves

http://www.sads.org.uk/technical_terms.htm

sympathectomy totally ablates regional spinal cord blood flow

We conclude that adrenalectomy near-totally ablates the hypothermia-associated increase in RSCBF measured in intact rats and that abdominal sympathectomy totally ablates it. This evidence complements morphological evidence for adrenergic innervation of the spinal cord vasculature.

http://ajpheart.physiology.org/cgi/content/abstract/260/3/H827

Transverse myelitis

Transverse myelitis is a neurological disorder caused by an inflammatory process of the grey and white matter of the spinal cord, and can cause axonal demyelination.
In some cases, the disease is presumed to be caused by viral infections or vaccinations and has also been associated with spinal cord injuries, immune reactions, schistosomiasis and insufficient blood flow through spinal cord vessels. Acute myelitis accounts for 4 to 5 percent of all cases of neuroborreliosis.^[1] Symptoms include weakness and numbness of the limbs as well as motor, sensory, and sphincter deficits. Severe backpain may occur in some patients at the onset of the disease.

http://en.wikipedia.org/wiki/Transverse_myelitis

One patient with documented transection of the cord above T5 behaved like subjects after surgical sympathectomy 

 

Increase in blood flow is generally followed by a rise in skin temperature but decrease in blood flow in response to the Gibbon-Landis procedure after sympathectomy is not necessarily accompanied by a fall in surface temperature. This poor correlation between skin temperature and blood flow confirms the previous report of Hoobler and co-workers and helps define the limits of usefulness of measurements
of skin temperature as an index of blood flow to the extremity.

The vasomotor responses to the Gibbon-Landis procedure (reflex response to warming) were studied in hemiplegic patients, subjects with "high transection" of the cord, and in sympathectomized patients.

One patient with documented transection of the cord above T5 behaved like subjects after surgical sympathectomy.
Of 11 sympathectomized limbs tested for vasodilatation in response to the Gibbon-Landis procedure, 4
showed no response, while 7 responded with decrease in blood flow (vasoconstriction).

Vasomotor Responses in the Extremities of Subjects with Various Neurologic Lesions
I. Reflex Responses to Warming
By WALTER REDISCH, M.D., FRANCISCO T. TANGCO, M.D., LOTHAR WERTHEIMER, M.D.,
ARTHUR J. LEWIS, M.D., J. MURRAY STEELE, M.D.
1957;15;518-524 Circulation

inhibition of sympathetic activity and a possible impairment of endothelial function

Alterations in skin microcirculation induced by brachial plexus block can be evaluated by wavelet transform of the laser Doppler flowmetry signal. Brachial plexus block reduces the oscillatory components within the 0.0095- to 0.021- and 0.021- to 0.052-Hz intervals of the perfusion signal. These alterations are related to inhibition of sympathetic activity and a possible impairment of endothelial function.

Anesthesiology:

September 2006 - Volume 105 - Issue 3 - pp 478-484

Clinical Investigations

Endothelial dysfunction, or the loss of proper endothelial function, is a hallmark for vascular diseases, and often leads to atherosclerosis.
http://en.wikipedia.org/wiki/Endothelium

'Emotional' sweating regulated by neocortex and limbic cortex

Careful observations showed that the forearm sweating responded diversely to various mental stimuli, unlike the palmar sweating whose response was always an increase. Mental arithmetic, mental testing and physical exercise caused an immediate increase in the palmar sweating but often elicited a transient decrease in the forearm sweating, whereas pain, noise, and emotional stimuli consistently provoked an increase of sweating on the forearm as well as on the palm. These observations suggest that the activities of higher centers, presumably involving neocortex and limbic cortex, exert various influences on the central mechanisms of palmar and generalized sweating.
Jpn J Physiol. 1975;25(4):525-36.
http://www.ncbi.nlm.nih.gov/pubmed/1206808 

90% may experience Gustatory sweating after surgery for Hyperhidrosis

Some individuals (up to 90%) may experience another type of sweating that is increased while eating or smelling certain foods (gustatory sweating) (Hornberger).Source: Medical Disability Advisor

Publish Post

http://www.mdguidelines.com/sympathectomy

 

Changes in cerebral capillary bed

Changes in cerebral capillary bed

Changes in the cerebral capillary bed following cervical sympathectomy,' Arch. Neurol. and Psychiat., 1929, 21, 1102.
Tracy J. Putnam
The Cerebral Circulation: Some New Points in its Anatomy, Physiology and Pathology
J Neurol Psychopathol, Jan 1937; s1-17: 193 - 212.

Permeability and Sympathetic Nervous System

In dogs, cats, and rabbits sympathectomy reduces the penetration of dye from the blood through the synovial membrane of the knee joint.
J Neurol Psychiatry, Apr 1941; 4: 147 - 162.

Observations during lobotomy applied to patients for treatment of palmar sweating

J. Neurol. Neurosurg. Psychiatry, Aug 1954; 17: 196 - 203.
......similar serial observa- tions on patients undergoing other intracranial operations. One patient undergoing a two-stage lumbar sympathectomy for hypertension was studied in detail. Following both operations she failed to show any marked rise in skin resistance......

Alick Elithorn, Malcolm F. Piercy, and Margaret A. Crosskey
A PERSISTING CHANGE IN PALMAR SWEATING FOLLOWING PREFRONTAL LEUCOTOMY

Increased sensitivity to insulin following sympathectomy

the increased insulin tolerance seen in patients during the immediate post-operative period after lumbo-dorsal sympathectomy is followed by a secondary stage of increased sensitivity to the drug.

E. Marley ALTERED RESPONSE TO SMALL DOSES OF INSULIN ASSOCIATED WITH ELECTROPLEXY AND HYPOGLYCAEMIC THERAPIES J. Neurol. Neurosurg. Psychiatry, Feb 1956; 19: 57 - 61.

Sprouting following sympathectomy- recurrence of symptoms

They showed that recovery of function after partial sympathectomy in cats depends, not on hypersensitivity, but on collateral sprouting of the surviving sympathetic fibres.
G. F. M. Russell

J. Neurol. Neurosurg. Psychiatry, Nov 1958; 21: 290 - 296.

Auto-regulation after sympathectomy

sympathectomy changes the position of upper and lower limits of auto- regulation but not the basic ability to autoregulate per se (Fitch)

J. D. Pickard, D. P. J. Boisvert, D. I. Graham, and W. Fitch Late effects of subarachnoid haemorrhage on the response of the primate cerebral circulation to drug-induced changes in arterial blood pressure J. Neurol. Neurosurg. Psychiatry, Oct 1979; 42: 899 - 903.

Oedema associated with the interruption of preganglionic sympathetic tract

J. Neurol. Neurosurg. Psychiatry, Mar 1992; 55: 232 - 233.
......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 pressure.....

Dilation of major cerebral arteries and cranial noncerebral vasodilation following sympathectomy

Headache Following Cervical Sympathectomy
Headache. 43(4):410-414, April 2003.
Spierings, Egilius L. H. MD, PhD

Abstract:
Background: A patient developed severe, continuous, unilateral headache that was "vascular" in nature, following cervical sympathectomy.

Objective: To determine the changes in cranial blood flow in the cat following lesioning and stimulation of the cervical sympathetic nerve.

Method: Carotid blood flow was determined by electromagnetic flowmetry and its tissue distribution by intra-arterial injection of 15-[mu]m radioactive microspheres.

Results: Following sympathetic lesioning, an increase in carotid blood flow was observed and reversed with stimulation. The distribution of carotid blood flow changed for the brain only, maintaining relatively constant tissue perfusion.

Conclusion: An increase in cerebral blood flow could not have accounted for the sympathectomy-induced headache. Dilation of major cerebral arteries and cranial noncerebral vasodilation probably constitutes its mechanism.

pituitary secretions of ACTH and TSH after sympathectomy

Cervical sympathectomy affects adrenocorticotropic hormone and thyroid-stimulating hormone in rats

Journal	Journal of Anesthesia
Publisher	Springer Japan
ISSN	0913-8668 (Print) 1438-8359 (Online)
Issue	Volume 10, Number 3 / September, 1996

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.

remarkable changes in the nerves that remain

Chemical denervation and selected ganglionectomy studies have shown that loss of sympathetic or sensory innervation induces remarkable changes in the nerves that remain.

Sympathectomy. Unilateral removal of the SCG results in the reinnervation of the denervated cerebral vessel by sprouting nerves from the contralateral ganglion (Kahrstrom et al. 1986). Following chronic guanethidine sympathectomy there is a complete depletion of sympathetic cotransmitters NA and NPY from the dura mater but an increase in the expression of NPY in non-sympathetic axons (lacking small dense-cored vesicles) supplying cerebral vessels and the iris (Mione at al. 1990). The source of increased cerebrovasular NPY is thought to be preexisting parasympathetic cranial ganglia which normally express both NPY and VIP (Gibbins and Morris 1998).
Indeed, sympathectomy-induced DBH-immunoreactivity in the sphenopalatine (parasympathetic) ganglion occurs at the same time as a loss of VIP-immunoreactivity (Fan and Smith 1993). In the cerebral and uterine artery, loss of sympathetic nerves also leads to increased DBH-immunoreactivity in non-sympathetic nerves that lack TH and NA (Morris et al. 1991).

The loss of sympathtetic neurones and nerve fibres is also accompanied by striking increases in sensory innervation. This has been attributed to increased availability to NGF (as there are no sympathetic nerves with which to compete for uptake) which promotes the growth of sensory nerves (Kessler et al. 1983)

In the lung, sympathectomy induced a marked increase in CGRP-immunoreactive nerve density around the airways, and blood vessels.

The Autonomic Nervous System. Part I. Normal Functions by O. Appenzeller (Hardcover - Dec 1, 1999)

Category: Neurology & Clinical Neurophysiology

Publication Date: 1999-12-16 Publisher: Elsevier - Health Sciences Div

Ultrastructural changes in the pineal gland

H. J. Romijn¹

(1)	Present address: Department of Electron Microscopy, Netherlands Central Institute for Brain Research, Amsterdam, The Netherlands

Received: 3 March 1975

Summary The ultrastructure of the rabbit pineal gland was investigated after sympathectomy (extirpation or decentralization of the superior cervical ganglia), parasympathectomy, continuous illumination and continuous darkness. The similarity of the ultrastructural changes in the light pinealocytes occurring after sympathectomy and after continuous illumination was striking. It is supposed that these changes have a common cause,viz. the lack of free noradrenaline, the pinealotropic neurotransmitter.

The smooth endoplasmic reticulum present in the terminals of the offshoots of the light pinealocytes is possibly involved in pineal indoleamine synthesis.

Journal of Neural Transmission
SpringerLink DateTuesday, March 29, 2005

Denervated heart does not respons as effectively as it should

Somatic effectors are dependent on their innervation to maintain structural and functional integrity. When denervated, they eventually atrophy. This is the fate of denervated voluntary muscles as noted in a lower motor neuron paralysis.
Denervated involuntary muscles, cardiac muscle, and glands continue to function. For example, the transplanted heart may function reasonably well. However, when deprived of autonomic nervous system influences, these effectors are abnormal in that they do not respond as effectively as they should to satisfy the changind demands of the organism.

The Human Nervous System

Structure and Function

Noback, C.R.; Ruggiero, D.A.; Demarest, R.J.; Strominger, N.L. (Eds.)

2007, 416 p. 178 illus., Softcover

ISBN: 978-1-58829-040-3

Mia: Please note, that with heart transplants both, sympathetic and parasympathetic influences are disrupted , so while there is denervation, there is no obvious imbalance between these. In sympathectomy, only the sympathetic nerves are cut, and the parasympathetic influence is predominant, whic will result in slowing of the heart.

Reduced Heart Rate Variability and Increased C-reacitve protein - predicts death and myocardial infarction

Increased C-reactive protein (CRP) and reduced heart rate variability (HRV) both indicate poor prognosis. An inverse association between HRV and CRP has been reported, suggesting an interaction between inflammatory and autonomic systems. However, the prognostic impact of this interaction has not been studied. We thus investigated the prognostic impact of CRP, HRV and their combinations.

Conclusions: The combination of CRP and HRV or heart rate (HR) predicts death and myocardial infarction with synergism, indicating interaction between inflammatory and autonomic systems with a prognostic significance.

Journal of Internal Medicine. 260(4):377-387, October 2006.
SAJADIEH, A. 1; NIELSEN, O. W. 1; RASMUSSEN, V. 2; HEIN, H. O. 3; HANSEN, J. F. 1

Sympathectomy is known to alter immunity

Chemical Sympathectomy, as well as manipulation of the autonomic nervous system, is known to alter lymphocyte dependent immunity.
The stress induced by autonomic dysregulation after SCI, and especially by episodes of autonomic dysreflexia, may well be an important cause of immune suppression in this group.

Neurologic events are known to affect immunologic function indirectly, through the pituitary adrenal axis, and through endocrine and neuropeptide regulation. Stress induces the release of adrenocorticotrophic hormone from the pituitary. This induces the release of immuno-suppressive glucocorticoids. In addition, the adrenal medulla releases catecholamines that alter leukocyte migration and lymphocyte responsiveness. Other hormones, including insulin, thyroxin, growth hormones, samostatin, and the sex hormones modulate T- and B-cell functions in complex ways. A number of abnormalities in endocrine function accompany SCI. Abnormal endocrine physiology involving sex hormones, aldosterone, catecholamines, and methylhydroxymandelic acid have been described.
Spinal Cord Medicine: Principles and Practice Spinal Cord Medicine: Principles and practiceby Vernon W. Lin, Diana D. Cardenas, Nancy C., MD Cutter,
Published by Demos Medical Publishing, LLC. 2002

efficacy ranging from 13% to 80% ?

Lumbar sympathetic blockade is indicated for diagnosis, prognosis, and therapy of painful and other conditions presumably associated with sympathetic nervous system dysfunction. Anatomy of the lumbar sympathetic chain and the rationale for the block are essential to know before performing the block. Different techniques have been described for the lumbar sympathetic blockade, with efficacy ranging from 13% to 80%, which varies according to the initial patient pathology. Genito-femoral neuralgia occurs in about 5% of patients after neurolytic block. Other potential complications are infection, hematomas, and somatic nerve damage. Copyright © 2001 by W.B. Saunders Company

Techniques in Regional Anesthesia and Pain Management, Volume 5, Issue 3, Pages 99-101
N.Mekhail, O.Malak

cervical sympathectomy resulted in a rapid degeneration in some of the cells in the sinuatrial and atrioventricular nodes

J Anat. 1984 October; 139(Pt 3): 449–461.

PMCID: PMC1165060

Copyright notice

An ultrastructural study of the effects of right cervical sympathectomy on the sinuatrial and atrioventricular nodes in the heart of the monkey (Macaca fascicularis).

S S Tay, W C Wong, and E A Ling

This study describes the ultrastructural changes in the sinuatrial and atrioventricular nodes of the heart of the monkey (Macaca fascicularis) after right cervical sympathectomy. Obvious changes in the nodal cells were seen one day after operation. Numerous glycogen particles grouped together to form electron-dense patches containing vacuoles in the cytoplasm. At three days after operation, intracellular organelles exhibited fragmentation and dissolution. By five and seven days after operation, the affected cells were vacuolated and some were swollen and appeared to have degenerated. Simultaneously, there was massive infiltration of macrophages were present nodal tissues. Axon profiles and terminals showing various degrees of degeneration were present in the vicinity of the nodal cells throughout the period of study. It is concluded that right cervical sympathectomy resulted in a rapid degeneration in some of the cells in the sinuatrial and atrioventricular nodes.

Cervical sympathectomy causes photoreceptor-specific cell death in the rat retina

There was a significant reduction (30%) in photoreceptor numbers in the sympathectomized eye. This loss was due to apoptosis, as there was over a doubling in apoptotic cell numbers after sympathectomy. This loss of photoreceptors in the sympathectomized eye resulted in a significantly reduced width of the outer nuclear layer of the retina when compared to the contralateral eye. Increased glial fibrillary acidic protein (GFAP) staining was also noted after sympathectomy in the ganglion cell layer with streaking toward the bipolar cell layer. These results suggest that loss of sympathetic innervation may cause significant changes to the physiology of the choroid.

Autonomic Neuroscience, Volume 120, Issue 1, Pages 46-51
J. Steinle, N. Lindsay, B. Lashbrook