The effects of a continuous infusion of etomidate on cerebral function, metabolism, and hemodynamics and on the systemic circulation were examined in six dogs. The infusion rate of etomidate was progressively increased at 20-min intervals from 0.02 to 0.4 mg · kg−1· min−1for 2 h. Cerebral oxygen consumption (CMRO2) decreased until there was cessation of neuronal function as reflected by the onset of an isoelectric EEG. This occurred during an infusion of 0.3 mg · kg−1· min−1etomidate when the animals had received a total of 10.7 mg · kg−1over 91 min. At this time the CMRO2was 2.6 ml · min−1· 100 g−1, 48% of control. Thereafter, despite continued administration of etomidate to a total dose of 21.4 mg · kg−1CMRO2did not decrease further. Cerebral blood flow (CBF) decreased in association with a marked increase in cerebrovascular resistance but was independent of changes in CMRO2CBF decreased precipitously from 145 ± 23 to 72 ± 6 ml · min−1· 100 g−1during the lowest infusion rate of 0.02 mg · kg−1· min−1etomidate and stabilized at 34–36 ml · min−1· 100 g−1during an infusion rate of 0.1 mg · kg−1· min−1· CBF remained at this level despite the continued administration of etomidate and a further decrease in CMRO2· Etomidate produced physiologically minor but statistically significant changes in the systemic hemodynamic variables. Assays of cerebral metabolites taken at the end of the infusion revealed a normal energy state and a very mild but significant increase in cerebral lactate to 1.49 μmol · g−1. We conclude that etomidate is a potent, direct cerebral vasoconstrictor that appears to be independent of its effect on CMRO2and that the cerebral metabolic effects of etomidate are secondary to its effect on neuronal function, with little if any direct or toxic effects on metabolic pathways.