The cerebral metabolic effects of isoflurane at and above concentrations that suppress cortical electrical activity.

The effects of 1.4-6.0% end-expired isoflurane on cerebral metabolism and hemodynamics were examined in dogs. A dose-related decrease in cerebral oxygen consumption (CMRO2) occurred until there was suppression of cortical electrical activity as reflected by the onset of an isoelectric electroencephalogram. This occurred at an end-expired concentration of 3% isoflurane when the mean CMRO2 was 2.02 ml X 100 g-1 X min-1. Thereafter, increasing concentrations of isoflurane to 6% had no further effect on the CMRO2. Brain biopsies taken at the end of the study revealed normal concentrations of ATP and phosphocreatine and a normal energy charge. Despite a normal cerebral energy state, there was a mild, dose-related, cerebral lactic acidosis (up to 2.84 mumol/g) that accompanied a mild systemic acidosis. It is concluded that the cerebral metabolic changes produced by isoflurane are secondary to an effect on cortical electrical activity, that abolition of this activity can be produced in dogs by a clinically relevant concentration of isoflurane (3%) without marked systemic hemodynamic effects, and that concentrations of isoflurane necessary to abolish cortical activity have no direct toxic effect on cerebral metabolic pathways.