We investigated the effects of isoflurane-induced hypotension on global cerebral blood flow (CBF), cerebral metabolic rate for oxygen (CMRO,), and the balance between cerebral oxygen supply and demand in 8 mongrel dogs. After endotracheal intubation, anesthesia was maintained with nitrous oxide (50%)-oxygen (50%)-fentanyl (2u/kg/hour). Ventilation was controlled to normocapnia. Mean arterial pressure (MAP) was lowered to 60 mmHg with inhalation of isoflurane. CBF was measured directly using sagittal sinus outflow method before (prehypotension), during (hypotension), and after (posthypotension) isoflurane-induced hypotension. Concomitantly, arterio-sagittal sinus venous oxygen content differen- ce was measured to calculate CMRO2. During hypotension, CBF and CMRO, were measured at 20 minutes after MAP was lowered to 60 mmHg and maintained stably. The time to induce hypotension was 8.6±6.1 (mean±SD) min. Mean inspired isoflurane concentra tion to induce desired hypotension was 3.1±0.9 vol%. The time to recover from hypotension was 28.6±7.7 min. MAP and heart rate were reduced significantly during hypotension (p<0.05, respectively) and returned to prehypotensive values during posthypotension. CBF was not changed between three peroiods. CMRO2 was reduced significantly during hypotension (6.5±1.2 vs 4.3±0.8ml/100/g/min, mean±SD, p<0.05) and returned to prehypotensive values during posthypotension. The percentage of CMRO2 reduction from prehypotension to hypotension (% CMRO2 reduction) was 32.5±12.9%. CBF/CMRO2 ratio was increased significantly during hypotension (12.8±3.3 vs 18.2±6.1, mean±SD, p<0.05) and lowered to prehypotensive values during posthypotension. Isoflurane-induced hypotension maintained CBF and reduced CMRO2 and therefore favorably influenced the balance between the global cerebral oxygen supply and demand. In conclusion, isoflurane induced-hypotension may be a safe and effective technique in view of the balance of the global cerebral oxygen supply and demand.