The influence of etomidate on regional cerebral function as reflected by regional cerebral glucose utilization (rCMRGlc) was studied. Three experiments were performed. In the first, rats had both left femoral vessels cannulated and were placed in restraining cages. Etomidate was infused intravenously (12 mg/kg) at a rate of 6 mg · kg−1· min−1. This large dose had a modest effect on blood pressure and heart rate, which could be explained by the elimination of stress in restrained rats, and no effect on body temperature, PaO2, PaCO2, orpH. A second group of rats were used to determine the effect of etomidate on the ratio of brain glucose to plasma glucose, which is necessary for calculating rCMRGlc. In the third experiment rCMRGlcwas measured in unstressed rats. The rats were anesthetized with an intravenous dose of 1, 2, 6, or 12 mg/kg etomidate infused at a rate of 6 mg · kg−1· min−1. Etomidate had a marked effect on glucose consumption in many, but not all, cerebral structures. The forebrain (telencephalon and diencephalon) was most affected (–25% to –35%) while the hindbrain was minimally affected. There was no demonstrable dose dependency; 1 mg/kg depressed rCMRGlcas much as 12 mg/kg. The pattern of rCMRGlcdepression is in accord with the minimal effects observed on physiologic variables and similar to that caused by the steroid anesthetic Althesin,® although the depression seen was not as severe. The pattern of metabolic depression produced by etomidate differs markedly from that produced by barbiturates, which affect all brain regions to a similar degree. The possibility is discussed that the anesthetic effect of etomidate may be mediated by receptors.