Cervical Sympathectomy Research Articles

The evolution of surgery for the treatment and prevention of stroke. The Willis Lecture.

Thomas Willis, the man for whom this lecture is named, was an Englishman and a leading neuroanatomist of the 17th century. Born in 1621, he attended Oxford University, graduating from Christ Church College in 1639. While still at Oxford, he became Sedleian Professor of Natural History in 1660. He did much experimental work with his associate Richard Lower. He performed injection experiments on cadavers and noted that if he injected the carotid artery on one side, the dye solution would come forth from the carotid on the opposite side. In 1664 Willis published his monumental work Cerebri Anatome , the most complete and accurate account of the nervous system that had hitherto appeared. In it he contributed the term “neurology” to medicine, a word derived from the Greek, meaning “sinew,” “tendon,” or “bowstring.” The word was translated and introduced into the English language in 1681 in Samuel Pordage's translation of Willis' work. Cerebri Anatome contains a classification of the cerebral nerves, the first description of the eleventh nerve, and a description of the hexagonal network of arteries at the base of the brain that we know as the circle of Willis. Although others had described the circle before Willis, he was the first to grasp its physiological and pathological significance. He records the clinical histories of two patients in whom he suggests that the anatomic configuration of the arteries at the base of the brain could prevent apoplexy. The book was illustrated by Christopher Wren, an associate of Willis at Oxford, later to become England's leading architect and designer of St Paul's Cathedral, numerous other English churches, and many historic secular buildings. Willis moved to London in 1666 and acquired the largest fashionable practice of his day. He continued his careful clinical observations and made a number of other important …

Cervical sympathectomy inhibits axonal transport of gonadotropin-releasing hormone during continuous exposure to light in male rats

Cervical sympathectomy inhibits axonal transport of gonadotropin-releasing hormone during continuous exposure to light in male rats

The role of adenosine in functional hyperaemia in the coronary circulation of anaesthetized dogs.

1. The aim of this investigation was to determine the contribution of adenosine to coronary active hyperaemia in the dog denervated heart by using adenosine deaminase. 2. Beagles were anaesthetized with thiopentone sodium (500 mg, I.V.) and chloralose (100 mg kg-1, LV.) and artificially ventilated. The hearts were denervate by bilateral cervical vagotomy and cardiac sympathectomy. Blood samples were collected from the coronary sinus via a cannula passed through the right external jugular vein. The anterior descending or circumflex branch of the left coronary artery was cannulated and perfused with blood from the left subclavian artery under systemic blood pressure through an electromagnetic flow probe and a perfusion circuit. The heart was paced (3 V, 0.2 ms and a suitable frequency) via two electrodes attached to the right atrium from 109 +/- 7.3 to 170 +/- 9.8 beats min-4 (means +/- S.E.M.) for 3-4 min, first during an infusion of the solvent, and then during an infusion of a solution of adenosine deaminase (5 U kg-1 min-1) into the circuit. 3. In seventeen tests in eight dogs, infusion of adenosine deaminase did not cause a significant change in the basal coronary blood flow nor in the immediate increase (within 10s) in blood flow induced by pacing the heart from its basal rate to 170 beats min-1. However, adenosine deaminase did cause a significant attenuation by 58 +/- 5.2% (P < 0.05) of the increase in coronary blood flow induced at 3-4 min of pacing from 31 +/- 4.6 to 43 +/- 5.8 ml min-1 (100 g cardiac tissue)-1. Concomitantly, the pacing-induced increase in coronary vascular conductance (from 0.41 +/- 0.08 to 0.54 +/- 0.12 ml min-1 (100 g)-1 mmHg-1) was reduced by 75 +/- 6.6% (P < 0.02) and the increase in myocardial O2 consumption (from 13 +/- 3.5 to 21 +/- 4.2 ml min-1 (100 g)-1) was reduced by 50 +/- 12% (P < 0.05) but without significant changes in oxygen extraction or myocardial contractility. 4. The results show that although adenosine is unlikely to play a significant role in the regulation of the basal coronary blood flow, it can play a major role in the coronary active (functional) hyperaemia induced by atrial pacing to a high rate in the denervated heart of anaesthetized dogs.

Cervical sympathectomy affects gonadotropin-releasing hormone, luteinizing hormone and testosterone in male rats.

To examine the effects of bilateral cervical sympathectomy on the secretion of gonadotropin-releasing hormone (GnRH), luteinizing hormone (LH) and testosterone (TS), 24 male rats were divided into four groups: control (C), light (L), sympathectomy (S), and light-sympathectomy (LS) groups. The C and S groups were kept under a 12-h light-dark cycle and the L and LS groups were kept under continuous light for 2 weeks. After 2 weeks, blood was collected and the rats were perfused with a fixative. GnRH neurons in the hypothalamus were stained immunohistochemically, and serum LH and TS levels were measured by radioimmunoassay. Although the difference in the number of GnRH neurons between the C and S groups was not significant, the L group was significantly lower than the C or LS groups. The serum LH and TS levels in the L group were higher than in the other groups. The present results suggest that continuous light increases GnRH secretion in the hypothalamus, followed by increased secretions of LH in the pituitary and TS in the testes, and bilateral cervical sympathectomy under continuous light inhibits these hormonal changes. However, a normal circadian rhythm does not affect gonadotropin secretion. Therefore, long-term and repeated stellate ganglion block may inhibit the increases of GnRH, LH, and TS secretions induced by continuous light.

Cervical sympathectomy affects gonadotropin-releasing hormone, luteinizing hormone and testosterone in male rats

Cervical sympathectomy affects gonadotropin-releasing hormone, luteinizing hormone and testosterone in male rats

An in vivo study of the effect of 5-HT and sympathetic nerves on transferrin and transthyretin mRNA expression in rat choroid plexus and meninges

Brain expression of transferrin (Tf) and transthyretin (TTR) mRNA has been demonstrated in different species. TTR being found only in the choroid plexus. We report here that both these mRNAs are also expressed in the meninges. In vitro studies have shown that Tf secretion by the rat choroid plexus is stimulated by 5-hydroxytryptamine (5-HT) while sympathetic nerves regulate different transport functions in the same tissue. We have used various in vivo models to study the neuroendocrine regulation of Tf and TTR mRNA expression in the choroid plexus and meninges. Destruction of the serotonergic nerves in the brain by either raphe nuclei lesion or intraventricular injections of 5,7-dihydroxytryptamine (5,7-DHT), which both decreased brain 5-HT levels significantly, did not affect Tf or TTR mRNA levels in choroid plexus and meninges, but increased TTR mRNA in liver. Intraventricular injection of 10 or 100 pmol 5-HT did not change the expression of these proteins in any of the tissues studied. Removal of the sympathetic innervation to the choroid plexus by cervical sympathectomy did not affect Tf or TTR mRNA levels in choroid plexus and liver, nor the incorporation of radioactive leucine into protein in various parts of the brain. In conclusion, our results do not support a regulatory role in vivo for neuronally derived 5-HT or sympathetic nerve activity on Tf and TTR mRNA expression in rat choroid plexus and meninges.

Cerebral vasoconstrictive response produced by chemical stimulation of the caudal ventrolateral medullary depressor area is mediated via the rostral ventrolateral medullary pressor area and the cervical sympathetic nerves

It was investigated that the cerebral blood flow (CBF) decrease response elicited by chemical stimulation of the caudal ventrolateral medullary depressor area (VLDA) is mediated via the rostral ventrolateral medullary pressor area (VLPA) and the cervical sympathetic nerve. The CBF was determined by radiolabeled microsphere technique in urethane (1.1–1.5 g · kg –1, i.p.) anesthetized Wistar rats. (i) Microinjection of l-glutamate (1.7 nmol) into the VLDA produced a significant ( P < 0.01) decrease in CBF from 64 ± 9 (mean ± SEM) to 48 ± 9 ml · min −1 · (100 g) −1 and a significant ( P < 0.01) increase in cerebrovascular resistance (CVR) from 1.7 ± 0.2 to 2.4 ± 0.4 mmHg per [ml · min −1 · (100 g) −1] in the cerebral cortex ipsilateral to the stimulated VLDA side ( n = 9). (ii) After cervical sympathectomy, l-glutamate was unilaterally microinjected into the VLDA. The CBF and CVR did not change significantly ( n = 10). (iii) After depression of the VLPA neurons with muscimol (GABA agonist), l-glutamate was unilaterally microinjected into the VLDA. The CBF and CVR did not change significantly ( n = 14). These results suggest that the pathway from the VLDA to control cerebral vessels may be mediated via the VLPA and the cervical sympathetic nerves.

Caudal ventrolateral medullary depressor area controls cerebral circulation via rostral ventrolateral medullary pressor area.

The cerebral blood flow (CBF) was determined by radiolabeled microsphere technique in urethane (1.1-1.5 g.kg-1, i.p.) anesthetized Wistar rats. Microinjection of L-glutamate (1.7 nmol) into the ventrolateral medullary depressor area (VLDA) produced a significant (P < 0.01) decrease in CBF from 64 +/- 9 (mean +/- S.E.M.) to 48 +/- 9 ml.min-1.(100g)-1 and a significant (P < 0.01) increase in cerebrovascular resistance (CVR) from 1.7 +/- 0.2 to 2.4 +/- 0.4 mmHg per [ml.min-1.(100g)-1] in the cerebral cortex ipsilateral to the stimulated VLDA side but not in other structures such as brain stem and cerebellum (n = 9). Cervical sympathectomy blocked the decrease in CBF and increase in CVR elicited by chemical stimulation of the VLDA (n = 10). Depression of the ventrolateral medullary pressor area (VLPA) neurons induced by microinjection of muscimol into the VLPA blocked the CBF decrease and CVR increase following chemical stimulation of the VLDA (n = 11). Microinjection of the vehicle solution into the VLDA had no effects on systemic and cerebral circulation (n = 7). These results suggest that a vasoconstrictor pathway to control cerebral vessels involves an excitatory projection from the VLDA to the VLPA and the changes in cerebral circulation are mediated by the cervical sympathetic nerves.

Changes in Serum Growth Hormone and Prolactin Levels, and in Hypothalamic Growth Hormone-Releasing Hormone, Thyrotropin-Releasing Hormone and Somatostatin Content, after Superior Cervical Sympathectomy in Rats

After bilateral superior cervical ganglionectomy (SCGx) of adult male rats, norepinephrine (NE) content of the medial basal hypothalamus (MBH) decreased significantly by 39-47% from 16 h to 7 days after surgery. During this time the levels of serum growth hormone (GH) and prolactin (PRL) and of MBH GH-releasing hormone (GRH), thyrotropin-releasing hormone (TRH) and somatostatin were measured by RIA. In sham-operated controls, serum PRL increased and serum GH decreased 16-24 h after surgery, attaining pre-surgical levels later on. In SCGx rats, significantly lower serum GH and PRL and higher MBH GRH and TRH content as compared to controls was observed 16-24 h after surgery, during the wallerian degeneration phase after SCGx. MBH somatostatin concentration decreased in SCGx rats 20 h after surgery. Two injections of the alpha 1-adrenoceptor blocker prazosin 45 and 90 min before sacrifice, alone or together with the beta-blocker propranolol, prevented the changes in MBH hypophysiotropic hormone content, as well as in serum GH and PRL levels, found in SCGx rats 20 h after surgery. Propranolol treatment did not affect hormone levels. Neither drug modified the decrease in MBH NE content observed after SCGx. The results argue in favor of the existence of physiologically relevant projections from superior cervical ganglion neurons to the MBH controlling hypophysiotropic hormone release.

The effects of unilateral cervical sympathectomy on mandibular growth in young rats: C. R. Chan, San Francisco, California: University of the Pacific, School of Dentistry, 1991

The effects of unilateral cervical sympathectomy on mandibular growth in young rats: C. R. Chan, San Francisco, California: University of the Pacific, School of Dentistry, 1991

Cervical sympathectomy reduces the heterogeneity of oxygen saturation in small cerebrocortical veins.

This study evaluated the hypothesis that the peripheral sympathetic nervous system is one of the factors increasing the heterogeneity of venous O2 saturation in selective brain regions. Regional cerebral blood flow and O2 saturation were determined in the anterior cortex, posterior cortex, and medulla of either sham-operated or bilaterally sympathectomized Long-Evans rats. Cerebral venous O2 saturations, indicating the balance between local O2 supply and consumption, were found to be significantly more heterogeneous in the sham-operated group. In the anterior cortex, the coefficient of variation [100(SD/mean)] for the sham-operated animals was 22.4%. Sympathectomy significantly reduced this heterogeneity in the anterior cortex through a reduction in the number of low O2 saturation veins (coefficient of variation 11.7%). Blood flow and O2 consumption in the anterior cortex were not different between groups. The effects of sympathectomy in the posterior cortex were similar to those in the anterior cortex. However, sympathectomy did not alter any measured variables in the medulla. Thus, bilateral superior cervical ganglionectomy reduced the heterogeneity of cerebrocortical venous O2 saturation by reducing the number of low O2 saturation veins in the rostral part of the brain.

Effect of cervical sympathectomy and hypoxia on the heterogeneity of O2 saturation of small cerebrocortical veins.

This study evaluated the hypothesis that the sympathetic nervous system was one of the factors increasing the heterogeneity of cerebrocortical venous O2 saturation and this heterogeneity would be greater during hypoxia when cervical sympathetic activity was elevated. Thirty-two male Long-Evans rats were either sham operated (n = 16) or received bilateral cervical sympathectomy (n = 16). One-half of the animals (n = 8) in each treatment were challenged by hypoxia (8% O2 in N2). Cerebral blood flow was determined in five brain regions with [14C]iodoantipyrine. Oxygen saturation was measured microspectrophotometrically in small cerebrocortical arteries and veins. The degree of hypoxic hyperemia was not significantly different between sham-operated and sympathectomized rats. Cortical venous O2 saturations, indicating the balance between O2 supply and consumption, were significantly more heterogeneous in the sham-operated group under both normoxic and hypoxic conditions. The coefficient of variation (CV = 100 x SD/mean) for the normoxic sham-operated animals was 24.9% and the average venous O2 saturation was 53.8%. During hypoxia, venous O2 saturation was significantly decreased to 43.1% without a change in CV (24.5%). Sympathectomy significantly reduced this heterogeneity through a reduction in the number of low O2 saturation veins (CV = 13.2%) under normoxic conditions and the effect was similar under hypoxic conditions (CV = 15.3%). In both sham-operated and sympathectomized groups, hypoxia elicited a significantly higher cerebrocortical O2 consumption. Thus, bilateral cervical sympathectomy improved the O2 supply in selective cerebrocortical regions with high O2 extraction. However, the effect of sympathetic innervation on the heterogeneity of cerebrocortical venous O2 saturation was not potentiated by hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute and Chronic Effects of Unilateral Cervical Sympathectomy on Nasal Allergy-like Symptoms Induced by Toluene Diisocynate in Guinea Pigs

The role of the sympathetic nervous system in nasal allergy was examined using guinea pigs with nasal allergy sensitized by 2,4-toluene diisocyanate (TDI). Nasal allergy-like symptoms were suppressed at the first TDI provocation after cervical sympathectomy. This finding suggests that the sympathetic nervous system contributes to the development of symptoms in nasal allergy. However, the inhibitory effect of sympathectomy gradually disappeared. The animals with chronic cervical sympathectomy were more prone to manifest nasal allergy-like symptoms induced by TDI. These findings suggest that compensatory activation of the parasympathetic nervous system in reaction to sympathectomy might exacerbate nasal allergy. The findings in the present study also provide an experimental basis for stellate ganglion block treatment of nasal allergy.

Radical microarteriolysis in the treatment of vasospastic disorders of the hand, especially scleroderma

Arterial spasm due to exaggerated sympathetic response is an important mechanism for Raynaud's phenomenon in scleroderma associated often with periadventitial scarring. The results of cervical sympathectomy have been unsatisfactory in the upper limb because of additional sympathetic pathways. Flatt therefore devised a distal sympathectomy by stripping the vessels of their adventitia over a short length of artery. The results of this operation were found by Wilgis in a large series to be poor in patients with scleroderma. A radical distal microarteriolysis including adventitia and surrounding scar is described and the results in 13 patients, 11 with scleroderma, are reported. Minimum follow-up is one year. All patients had relief from pain at rest and healing of painful ulceration. Mild recurrence of small ulcers was seen in only four patients.

A critical review of the afferent pathways and the potential chemical mediators involved in cardiac pain

There is considerable evidence that on the anterior surface of the heart (which is usually supplied by the left anterior descending and the proximal part of the left circumflex coronary arteries), sympathetic efferent reflexes characterized by tachycardia and/or hypertension predominate following experimental or pathological perturbations. These cardiovascular reflexes are accompanied by an increase in presumed nociceptive afferent traffic and, in pathological condition, by pain. In these experiments, there is generally no effect of vagotomy on afferent nerve traffic, and lower cervical and upper thoracic sympathectomies help provide relief from angina. On the other hand, experimental or pathological perturbations involving the inferior-posterior surface of the heart (supplied by the right and distal parts of the left circumflex coronary arteries), are characterized by vagal efferent reflexes, resulting in bradycardia and/or hypotension. These reflexes are accompanied by an increase in vagal afferent nerve traffic and, in pathological conditions, by pain. In these experiments, vagotomy generally abolishes such cardiovascular reflexes, and lower cervical and upper thoracic sympathectomies are not effective in the relief from angina. Although cardiac sympathetic afferents are unquestionably involved in the central transmission of nociceptive information from the heart, it is also likely that there is a contributing role from the vagus in cardiac pain. It is important experimentally to understand the natural stimulus that gives rise to angina. In the clinical situation, a decrease in coronary blood flow or an increase in the metabolic demands of the myocardium due to increased work are obvious precipitating factors which lead to myocardial ischemia. In the experimental situation, occlusion of the coronary arteries is often used as a stimulus which mimics myocardial ischemia. As people who frequently experience angina have varying degrees of coronary artery disease, it is difficult to accept that the state of the coronary arteries of the normal experimental animal bear any resemblance to the state of the coronary arteries under pathological conditions. That is, the gain of homeostatic reflexes, the basal concentrations of neuroactive substances in the plasma, the myocardium and the afferent terminals, the excitability of the afferents, access of chemical mediators (e.g. bradykinin, 5-HT, adenosine, histamine, prostaglandins, potassium, lactate), to afferents, and the overall function of the animal are all significantly different. We have no idea how control mechanisms have been altered in the person with severe coronary artery disease compared to the normal patient or the "normal" experimental animal.(ABSTRACT TRUNCATED AT 400 WORDS)

Regional quantitative permeability of blood-brain barrier lesions in rats with chronic renal hypertension

Blood-brain transfer constants for a small, neutral amino acid tracer, [ 14C]α-aminoisobutyric acid (AIB), were measured by quantitative autoradiography and image analysis in 15 individual brain structures of 2-kidney, 1-clip renal hypertensive rats (RHR) and age-matched normotensive cotrols (NR). Mean arterial presures (MAP) for 4 month-old RHR and NR were 182 ± 19 and 121 ± 3mmHg, respectively. Most brain structures in RHR had very low [ 14C]AIB transfer constants similar to those in NR (1–3 μl·g −1·min −1), indicate of normal blood-brain barrier (BBB) function. Focal lesions, however, having transfer contants 2–7x normal and measuring less than 1.7 mm 2 in area, appeared in RHR primarily in the cerebellar vermian and cerebral cortices. Chronic unilateral cervical sympathectomy did not influence the incidence or magnitude of BBB lesions in the denervated hemisphere of RHR. Acute arterial hypertension produced by systemic infusion of phenylephrine (elevation of MAP in RHR by 43%) increased the incidence and magnitude of lesions by 48% and 2–12x, respectively, although many brain regions in acutely hypertensive RHR retained normal permeability to [ 14C]AIB. The results demonstrate normal BBB permeability for much of the brain in chronic renal hypertension, with focal lesions having 7x or less the normal rate of bloodbrain transfer for a small physiological probe.

Sympathetic denervation and chronic serotonin uptake blockade by fluoxetine do not affect pineal gland 5-hydroxyindole acetic acid: evidence that oxidative deamination of pineal serotonin is a property of the pinealocyte.

This investigation tested the hypothesis that oxidative deamination of 5HT in the pineal gland occurs primarily in cellular compartments other than the pinealocyte (i.e., noradrenergic nerve terminals and glia). Following sympathetic denervation of the pineal gland by bilateral superior cervical sympathectomy, pineal levels of 5HT and its oxidative metabolite, 5HIAA, were measured by HPLC from samples collected at six time points over the 24 h photoperiod. The role of glia in 5HT deamination was further examined by chronic treatment with the 5HT uptake blocker, fluoxetine (10 mg/kg). Sympathectomy abolished the circadian rhythms of both 5HT and 5HIAA, but had no statistically significant effect on the ratio of 5HIAA/5HT compared to sham-operated and intact controls over the 24 h period. Pineal daytime levels of both 5HT and 5HIAA were unaffected by fluoxetine treatment. These findings indicate that the pinealocyte is an important cellular compartment for 5HT oxidative metabolism.

Reflex sympathetic dystrophy — The surgeon's role in management

It is important for vascular surgeons to be familiar with reflex sympathetic dystrophy because they may be called on to participate in the evaluation and treatment of patients with this syndrome. Over a 312-year period, 35 patients, initially evaluated by a team of pain experts, were referred for surgical sympathectomy for reflex sympathetic dystrophy. All patients had at least one positive diagnostic sympathetic block before they were considered for surgical sympathectomy. With use of this team approach and careful patient selection, excellent results were obtained in 74%, good results in 17%, and poor results in 9%. Three patients required a repeat cervical sympathectomy after initial surgery failed to relieve their symptoms. One patient required a contralateral lumbar sympathectomy after ipsilateral sympathectomy was unsuccessful. Better results were obtained in patients treated earlier in their course and with extended surgical sympathectomy. Patients not responding to initial sympathectomy should be evaluated for the presence of residual functional sympathetic tissue, and if this is identified, further sympathectomy by an alternate approach appears justified.

Feedback in the Rabbit's Central Circadian System, Revealed by the Changes in Its Free-Running Food Intake Pattern Induced by Blinding, Cervical Sympathectomy, Pinealectomy, and Melatonin Administration

Long-term records of the number of food approaches per 30 min were obtained from 16 rabbits in constant light and after blinding. Optic nerve sectioning usually resulted in a shortening of the free-running period (tau; mean reduction = -0.26 hr) of the oscillator governing the rabbit's food intake pattern. Subsequent resection of both superior cervical ganglia always reduced this tau (mean = -0.41 hr), and it could be further shortened (mean = -0.24 hr) by chronic administration of melatonin. These observations led to experiments in which the food intake of 15 blinded rabbits was recorded before and after pinealectomy. This always resulted in a lengthening of tau (mean = +0.27 hr), which was never seen after subtotal or sham pinealectomy in 10 other blinded animals (mean = -0.05 hr). Sympathectomy also reduced tau (mean = -0.50 hr) in the pinealectomized rabbits, whereas it induced a smaller reduction (mean = -0.29 hr) after sham pinealectomy. These results, together with previous observations on the effect of sympathectomy on the retinal "dark" discharge and on the influence of the latter upon the food intake pattern, indicate that the cervical sympathetic nerves may form part of three feedback loops for the rabbit's central circadian system. These have separate postganglionic pathways; there are also differences in the circadian phasing of their activities and in their effects on tau.

The effect of bilateral sympathectomy on noise induced temporary threshold shift

The cochlea is innervated by sympathetic nerves originating or passing the superior cervical ganglion. The termination of one type (the vascular independent) is in the habenular region close to the auditory nerve fibers, and the other, the perivascular type, is associated with blood vessels, particularly in the spiral vessel of the tympanic lip. Suggested functions have so far received partial evidence in the literature. Borg (1982) suggested the protective value of sympathectomy of the ear in noise. Our experiments further elaborate this protective value, as it was seen that bilateral cervical sympathectomy diminished the temporary threshold shift in awake, sound exposed GP.