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

Our aim in this study, performed using a closed cranial window preparation, was to investigate the effect of systemic pretreatment with dexmedetomidin e on cerebrovascular response to isoflurane or sevoflurane. After instrumen tation 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 dexme detomidine (0.5, 1.0, or 2.0 mu g/kg) (n = 6 each) IV. Animals were then ex posed to three different minimum alveolar anesthetic concentrations (MACs; 0.5, 1.0, and 1.5) of either isoflurane or sevoflurane. Cerebrovascular dia meters were measured at each stage. Pretreatment with dexmedetomidine decre ased pial vessel diameters. Both isoflurane and sevoflurane significantly d ilated both arterioles and venules in a concentration-dependent manner. Iso flurane- and sevoflurane-induced dilation of cerebral arterioles was signif icantly 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 sevofluran e. The vasodilation of cerebral pial vessels induced by isoflurane and sevo flurane could be attenuated by the systemic administration of dexmedetomidi ne, and this interaction between dexmedetomidine and volatile anesthetics s howed no evidence of dose-dependency. Implications: The systemic administra tion of dexmedetomidine attenuates the dilation of cerebral vessels induced by isoflurane and sevoflurane in pentobarbital-anesthetized dogs. This int eraction was not dependent on the clinical (0.5-2.0 mu g/kg) dose of dexmed etomidine and was not different between isoflurane and sevoflurane anesthes ia.