Isoflurane and sevoflurane induce vasodilation of cerebral vessels via ATP-sensitive K+ channel activation.

Abstract

Activation of adenosine triphosphate-sensitive K+ channels causes cerebral vasodilation. To assess their contribution to volatile anesthetic-induced cerebral vasodilation, the effects of glibenclamide, an adenosine triphosphate-sensitive K+ channel blocker, on the cerebral vasodilation induced by isoflurane and sevoflurane were studied. Pentobarbital-anesthetized dogs (n = 24) assigned to one of two groups were prepared for measurement of pial vessel diameter using a cranial window preparation. Each dog received three minimum alveolar concentrations (MAC; 0.5, 1, and 1.5 MAC) of either isoflurane or sevoflurane, and the pial arteriolar diameters were measured in the presence or absence of glibenclamide (10(-5) M) infused continuously into the window. Mean arterial pressure was maintained with phenylephrine. Furthermore, to assess the direct effect of isoflurane and sevoflurane on cerebral vessels, artificial cerebrospinal fluid was administered topically by being bubbled with isoflurane or sevoflurane. The blocking effect of glibenclamide on the vasoactive effects of these anesthetics also were evaluated. Isoflurane and sevoflurane both significantly dilated large (> or = 100 microm) and small (< 100 microm) pial arterioles in a concentration-dependent manner (6% and 10%, 3% and 8% for 0.5 MAC; 10% and 19%, 7% and 14% for 1 MAC; 17% and 28%, 13% and 25% for 1.5 MAC). Glibenclamide attenuated the arteriolar dilation induced by these anesthetics (not significant in isoflurane). Topical application of isoflurane or sevoflurane dilated large and small arterioles both in a concentration-dependent manner. Such vasodilation was inhibited completely by glibenclamide. The vasodilation of cerebral pial vessels induced by isoflurane and sevoflurane appears to be mediated, at least in part, via activation of adenosine triphosphate-sensitive K+ channels.