The Cerebral Metabolic Effects of Isoflurane at and above Concentrations that Suppress Cortical Electrical Activity

Abstract

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 O2 consumption (CMRO2) occurred until there was suppression of cortical electrical activity as reflected by the onset of an isoelectric EEG. This occurred at an end-expired concentration of 3% isoflurane when the mean CMRO2 was 2.02 ml/100 g per min. 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 .mu.mol/g) that accompanied a mild systemic acidosis. Evidently the cerebral metabolic changes produced by isoflurane are secondary to an effect on cortical electrical activity, abolition of this activity can be produced in dogs by a clinically relevant concentration of isoflurane (3%) without marked systemic hemodynamic effects and concentrations of isoflurane necessary to abolish cortical activity have no direct toxic effect on cerebral metabolic pathways.