The results of two studies on the effects of halothane and isoflurane in increasing end-tidal concentrations (0.25; 0.5; 1.0vol%) on the cerebral metabolic rate for oxygen and the cerebral blood flow are compared. Both studies were performed on baboons using the same experimental model. Cerebral blood flow was determined from a washout curve after the intracarotid injection of 133xenon. Halothane and isoflurane led to a dose-dependent decrease of the cerebral metabolic rate for oxygen. Increasing concentrations of halothane caused a decrease of cerebral oxygen consumption from 3.4 +/- 0.8 (baseline) to 2.9 +/- 0.8 (0.25vol%), 2.7 +/- 0.7 (0.5vol%) and 2.4 +/- 0.4 mlO2 100 g-1min-1 at 1.0vol%. The administration of isoflurane reduced the cerebral oxygen consumption significantly from baseline 3.7 +/- 1.0 to 2.9 +/- 0.9 at 0.25vol%, 2.6 +/- 0.6 at 0.5vol% and 1.8 +/- 0.8 mlO2 100 g-1min-1 with 1.0vol%. A significant, dose-independent reduction of the cerebral blood flow from 55.8 +/- 8.0 to 46.3 +/- 10.2 (0.25%) to 44.6 +/- 9.5 (0.5vol%) and 44.5 +/- 10.2 ml 100 g-1min-1 (1.0vol%) was observed with halothane. However, a dose-dependent decrease in calculated cerebrovascular resistance was seen at 1.0vol% of halothane. If mean arterial pressure was kept within the normal limits of cerebrovascular autoregulation by the administration of angiotensin-II-amid during 1.0vol% of halothane a marked increase in cerebral blood flow above the baseline value was observed. The lacking increase in cerebral blood flow observed at 1.0vol% of halothane without blood pressure support appeared to be caused by the low cerebral perfusion pressure rather than by vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)