The systemic and cerebral effects of hypotension induced with isoflurane were examined in 12 dogs. Hypotension to a mean arterial pressure of either 50 mmHg or 40 mmHg for 1 h was produced by 2.5 ± 0.1–2.9 ± 0.3% end-expired isoflurane anesthesia. Before and during the period of hypotension the following were measured or derived: arterial and pulmonary artery pressures; arterial, mixed venous, and sagittal sinus blood gases; cardiac output and cerebral blood flow; whole body and cerebral oxygen consumption; systemic and cerebral vascular resistance; intracranial pressure, serum lactate, and pyruvate concentrations; and blood glucose. At the end of the period of hypotension, brain biopsy specimens were taken for the determination of ATP, ADP, AMP, phosphocreatine, lactate, and pyruvate concentrations.Isoflurane-induced hypotension produced a significant decrease in systemic vascular resistance (27–43%) associated with a significant decrease in cardiac output (39–42%) and a smaller decrease in whole-body oxygen consumption (14–21%). Isoflurane also produced a significant decrease in cerebral oxygen consumption (40–44%) accompanied by a decrease in cerebral blood flow (60–62%). Following both the 40 and 50 mmHg periods of hypotension, the cerebral energy state was normal, indicating the preservation of normal aerobic metabolism. This differs from previous results obtained using a similar protocol, wherein trimethaphan-induced hypotension to 50 mmHg and trimethaphan, halothane, and nitroprusside-induced hypotension to 40 mmHg were associated with gross alterations in the cerebral energy state. Our failure to observe any detrimental effects of isoflurane-induced hypotension indicates that isoflurane may offer some advantage over other hypotensive techniques and is consistent with the concept that isoflurane offers a potential for cerebral protection.