Intravenous dexmedetomidine inhibits cerebrovascular dilation induced by isoflurane and sevoflurane in dogs.

UNLABELLED: Our aim in this study, performed using a closed cranial window preparation, was to investigate the effect of systemic pretreatment with dexmedetomidine on cerebrovascular response to isoflurane or sevoflurane. After instrumentation under pentobarbital anesthesia, 48 dogs were assigned to one of two groups: the isoflurane group or the sevoflurane group (n = 24 each). Twenty-four dogs received saline (n = 6) or one of three different doses of dexmedetomidine (0.5, 1.0, or 2.0 micrograms/kg) (n = 6 each) i.v. Animals were then exposed to three different minimum alveolar anesthetic concentrations (MACs; 0.5, 1.0, and 1.5) of either isoflurane or sevoflurane. Cerebrovascular diameters were measured at each stage. Pretreatment with dexmedetomidine decreased pial vessel diameters. Both isoflurane and sevoflurane significantly dilated both arterioles and venules in a concentration-dependent manner. Isoflurane- and sevoflurane-induced dilation of cerebral arterioles was significantly attenuated in the presence of dexmedetomidine. The dexmedetomidine-induced attenuation of the vascular responses was not dependent on the dose of dexmedetomidine and was not different between isoflurane and sevoflurane. The vasodilation of cerebral pial vessels induced by isoflurane and sevoflurane could be attenuated by the systemic administration of dexmedetomidine, and this interaction between dexmedetomidine and volatile anesthetics showed no evidence of dose-dependency. IMPLICATIONS: The systemic administration of dexmedetomidine attenuates the dilation of cerebral vessels induced by isoflurane and sevoflurane in pentobarbital-anesthetized dogs. This interaction was not dependent on the clinical (0.5-2.0 micrograms/kg) dose of dexmedetomidine and was not different between isoflurane and sevoflurane anesthesia.