Effect of General Anesthesia on Modulation of Sympathetic Nervous System Function

Abstract

Publisher Summary Halogenated anesthetics exhibit profound cardiovascular depressant effects that may be accompanied by a decrease in plasma catecholamine concentrations. Plasma norepinephrine (NE) concentrations have been used as a measure of sympathetic activity not only during anesthesia, but also in congestive cardiac failure and ischemia and to define sympathetic responses during vasodilator therapy. The inhalational anesthetics halothane, enflurane, and isoflurane and the intravenous anesthetic propofol produce marked sympathetic inhibition as measured by the decrease in NE spillover. It has been shown that NE spillover is a more accurate measure of sympathetic activity during anesthesia than is plasma NE concentration alone. The release of NE from peripheral sympathetic nerves is subject to presynaptic modulation by α -adrenergic, dopaminergic, and angiotensin receptors. A facilitative effect on peripheral noradrenergic sympathetic transmission has been demonstrated during and after exposure to epinephrine. The role of presynaptic β 2 –adrenergic receptors in facilitating NE release in humans is difficult to define because measurement of plasma NE is an inadequate measure of local NE release and β -agonist administration produces systemic effects with consequent vasodilation and hypotension with resultant secondary reflex stimulation of NE release. In addition, coinfusion of the β 1 – and β 1 –antagonist propranolol attenuated the isoproterenol-induced increase in local NE spillover.