Because less than 1 per cent of isoflurane is metabolized and there is no reductive metabolism or free-radical production, it is difficult to implicate isoflurane as a cause of hepatitis. Numerous animal and clinical studies have been performed, but none has produced evidence of hepatic dysfunction following isoflurane anesthesia. This has been ascribed to the chemical stability of isoflurane and the rapidity with which it is eliminated.
Studies of the effect of anesthetic agents on the liver are difficult to interpret as liver function tests are affected by many factors, such as surgical stress or hepatic arterial blood flow, as well as by the agent itself. Glutathione- S-transferase has been shown to be a more sensitive indicator of hepatocellular damage than the aminotransferases, and increases in this enzyme have been seen after halothane anesthesia but not following isoflurane anesthesia or sedation ( Howie.,..®t„al 1992).
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