This article reviews the direct action of sevoflurane on contractile response to noradrenaline in canine mesenteric arteries and veins focusing on the influence of the endothelium. Second, our several observations concerning cardioprotective effects with sevoflurane are also introduced with some references.
It is generally considered that sevoflurane is clinically vasodilator. However, studies in vitro have suggested that sevoflurane causes not only vasodilation but vasoconstriction, depending on the experimental situation. As results of our experiments, sevoflurane selectively impairs endothelium-dependent relaxation in canine mesenteric arteries by an oxygen free radical mechanism, mainly due to inactivation of EDRF/NO, and hypotension observed during sevoflurane anesthesia may due to its relaxing effect on veins and/or to inhibition of norepinephrine release from sympathetic nerve endings. It is also suggested that endothelium-intact arteries may protect against decreased arterial pressure by endothelium-dependent vasoconstriction, probably by inhibiting the release of basal EDRF/NO.
Lethal injury to heart can be dramatically blunted by brief conditioning periods of ischemia/reperfusion : a phenomenon called ischemic preconditioning. And brief exposure to a volatile anesthetic agent such as isoflurane and sevoflurane also protects the heart against subsequent ischemia/reperfusion injury. This phenomenon has been recognized as anesthetic preconditioning. Ischemic preconditioning and sevoflurane-induced preconditioning exert infarct size limiting effects through opening of mitochondrial KATP channels. Recent investigations have also demonstrated that sevoflurane pre- and post-conditioning reduce myocardial infarct size to a degree comparable to that achieved with ischemic preconditioning. Sevoflurane post-conditioning may be clinically applicable in situations where the potential for ischemia/reperfusion injury is of concern.
