Sympathectomy

Figure 3 Putative model for the mechanism by which biogenic amines stimulate CE secretion across the rabbit corneal epithelium. Epn = epinephrine Nep = norepinephrine Tim = Timolol Ser = serotonin Msg = methysergide Dop = dopamine Hal = haloperi-dol (E = (E-adrenoceptor AC = adenylate cyclase. The scheme is consistent with the observation that epithelial responsiveness to serotonin and dopamine can be blocked by their receptor antagonists haloperidol and methysergide, respectively, and by both timolol treatment and sympathectomy. The probable source of serotonin or dopamine is the sympathetic fibers that innervate the cornea. (From Ref. 284.)...

Madden, K.S. et al., Sympathetic neural modulation of the immune system. I. Depression of T cell immunity in vivo and in vitro following chemical sympathectomy, Brain Behav. Immun., 3, 72, 1989. 

Bellinger, D.L. et al., Aging and sympathetic modulation of immune function in Fischer 344 rats Effects of chemical sympathectomy on primary antibody response, J. Neuroim-munol., in press, 2005. 

Kelley, S.P. et al., Chemical sympathectomy has no effect on the severity of murine AIDS Murine AIDS alone depletes norepinephrine levels in infected spleen, Brain Behav. Im-mun., 16, 118, 2002. 

Sympathectomy and vagotomy alone or combined did not have any effect on radiation-induced emesis in dogs, while ablation of the AP abolished it [65-67], On the other hand, a triple intervention (ablation of area postrema and nerve sectionings) was required to prevent delayed emesis [65]. The rhesus monkey was similar to the dog, that is, the radiation-induced emesis was prevented by ablation of the area postrema [41]. 

Psychosurgery. Case series have been reported of patients with severe treatment resistant social anxiety disorder undergoing surgical procedures including capsu-lotomy and endoscopic transthoracic sympathectomy. Given the limited evidence... 

Pharmacology Bretylium tosylate inhibits norepinephrine release by depressing adrenergic nerve terminal excitability, inducing a chemical sympathectomy-like state. Bretylium blocks the release of norepinephrine in response to neuron stimulation. Peripheral adrenergic blockade causes orthostatic hypotension but has less effect on supine blood pressure. It has a positive inotropic effect on the myocardium. Pharmacokinetics Peak plasma concentration and peak hypotensive effects are seen within 1 hour of IM administration. However, suppression of premature ventricular beats is not maximal until 6 to 9 hours after dosing, when mean plasma concentration declines to less than 50% of peak level. Antifibrillatory effects occur within minutes of an IV injection. Suppression of ventricular tachycardia and other ventricular arrhythmias develops more slowly, usually 20 minutes to 2 hours after parenteral administration. 

J.P. Moak, B. Eldadah, C. Holmes, S. Pechnik, D.S. Goldstein, Partial cardiac sympathetic denervation after bilateral thoracic sympathectomy In humans. Heart Rhythm. 2 (2005) 602-609. 

Intra-arterial injection of thiopentone is a serious complication as crystals of the thiobarbiturate can form in the arterioles and capillaries, causing intense pain, vasoconstriction, thrombosis, and even tissue necrosis. Accidental intra-arterial injections should be treated promptly with intra-arterial administration of a vasodilator (papaverine 20 mg) and lignocaine (lidocaine) Note leave the needle/cannula in the artery), as well as a regional anaesthesia-induced sympathectomy (stellate ganglion block, brachial plexus block) and anticoagulation with intravenous heparin. The risk of ischaemic damage is much higher with a 5% solution and the use of this concentration is not recommended. 

A 39-year-old woman developed salbutamol-associated lactic acidosis (peak 7.8 mmol/1) during general anesthesia for planned thoracoscopic sympathectomy (1057). 

One of the distinguishing characteristics of uncomplicated neurogenic hypertension is its dramatic response to sympathectomy or to chemical blockade of the sympathetic nervous system. Complete sympathectomy results in an immediate reduction in the blood pressure to normal or to subnormal levels with a gradual return to normotensive or slightly higher levels over a period of 1 to 2 months (41, 48, 4)- Moderator nerve section or increased intracranial pressure usually fails to increase the blood pressure in completely sympathectomized animals and if a rise is elicited it is relatively slight and develops slowly (5, 27, 41) ... 

In contrast to neurogenic hypertension, the role of adrenergic factors in experimental renal hypertension is obscure. The sequence of events by which interference with renal hemodynamics leads to elevation of the systemic blood pressure has been carefully studied and has been shown to be independent of nervous mechanisms (see 11, 35). Sympathectomy does not prevent the development of renal hypertension and induces only slight and irregular reductions in pressure in renal hypertensive animals (3, 28, 55, 97). 

In human essential hypertension also, sympathectomy or blockade of the sympathoadrenal system brings about an equivocal response. There is little doubt that various degrees of surgical sympathectomy may produce a prolonged reduction in blood pressure in certain selected cases (43, 81, 82, 89), but the response is highly variable and the degree of benefit attributed to the procedures employed may depend to a considerable extent upon an evaluation of the natural course of the disease (see 79). 

Possible interrelationships of various hypertensive factors in renal (and perhaps essential) hypertension are diagramed in Figure 3. The highly variable response of renal and essential hypertension to sympathectomy or sympathetic blockade makes it impossible to present any diagram adequately covering all cases. 

Column C represents a case in which sympathetically mediated renal vascular tone is assumed to be a significant factor in maintaining the elevated pressure, and column D depicts possible changes in the few cases of human essential hypertension in which a continued fall in pressure is noted for some time after sympathectomy, perhaps also on the basis of altered renal blood flow. Column E represents a common result of sympathectomy or adrenergic blockade in renal and essential hypertension this result may or may not be preceded by some early fall in pressure such as illustrated in column C. 

Figure 2. Possible Contributions to Maintenance of Systemic Arterial Pressure during Neurogenic Hypertension and Its Subsequent "Cure by Sympathectomy or Adrenergic Blockade A. Normal...

C to E. Sequential stages in recovery of blood pressure after sympathectomy. Pressure may stabilize at either D or E... 

Guanethidine increases sensitivity to the hypertensive effects of exogenously administered sympathomimetic amines. This results from inhibition of neuronal uptake of such amines and, after long-term therapy with guanethidine, supersensitivity of effector smooth muscle cells, in a fashion analogous to the process that follows surgical sympathectomy (see Chapter 6 Introduction to Autonomic Pharmacology). 

MODIFICATIONS OF THE METHOD Either chemical (6-hydroxydopamine, reserpine) or surgical (section of hypogastric nerves) sympathectomy produces a picture of detrusor hyperreflexia and urine dropping, mimicking cystometric finding in human disease (Maggi et al. 1987a). 

Thoenen H, Tranzer JP (1968) Chemical sympathectomy by selective destruction of adrenergic nerve endings with 6-hydroxydopamine. Naunyn-Schmied. Arch Pharmacol 261. 211-288. 

Patients taking certain systemic medications are also more sensitive to the pressor effects of phenylephrine. In individuals taking atropine, the pressor effect of phenylephrine is augmented, and tachycardia can occur. Tricyclic antidepressants and monoamine oxidase (MAO) inhibitors also potentiate the cardiovascular effects of topical phenylephrine. The concomitant use of phenylephrine is contraindicated with these agents, even up to 21 days after cessation of MAO inhibitor therapy. Similarly, patients taking reserpine, guanethidine, or methyldopa are at increased risk for adverse pressor effects from topical phenylephrine because of denervation hypersensitivity accompanying the chemical sympathectomy. 

Contraindications to the topical use of hydroxyamphetamine for routine mydriasis are similar to those to phenylephrine. Because of its tachyphylaxis and ineffectiveness in postganglionic denervation, however, hydroxyamphetamine may be a safer mydriatic for use in patients with insulin-dependent diabetes, idiopathic orthostatic hypotension, or chemical sympathectomy produced by therapy with systemic guanethidine, reserpine, or methyl-dopa. Thus hydroxyamphetamine seems to be less strongly contraindicated than phenylephrine for certain high-risk patients. 

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