Studies of cerebral circulation and gaseous metabolism were performed in six healthy young volunteers during anesthesia induced with thiopental and maintained with nitrous oxide andd-tubocurarine. The blood thiopental level was very low when measurements were made, and intravenousd-tubocurarine has been shown not to affect cerebral flow or metabolism. Therefore 70 per cent nitrous oxide was probably the agent chiefly responsible for the changes observed. When Paco2was normal, cerebral blood flow remained normal, but cerebral oxygen uptake decreased 23 per cent. About one third of this decrease was caused by a small decline in body temperature, with the remainder most likely owing to nitrous oxide. When mean arterial Pco2was decreased to 18.3 mm. of mercury, cerebral blood flow was halved, and mean jugular venous Pco2declined to 19.8 mm. of mercury, a level generally assumed to be associated with suboptimal cerebral oxygenation. However, cerebral metabolic rate for oxygen did not decrease further at this low Paco2.