During hemorrhagic shock, liver is susceptible to ischemia and decreased hepatic energy charge results in decreasing arterial ketone body ratio(AKBR). Reperfusion after hemorrhagic shock can greatly amplify the generation of toxic oxygen metabolites. As a result, the fluxes of these highly toxic metabolites can overwhelm the endogenous antioxident defense mechanisms and lead to tissue injury. In order to observe the effect of glutathione(GSH) on the AKBR in hemorrhagic shock, dogs(n=16) were anesthetized with 1% enflurane in 02. We pretreated glutathione (100 mg/kg) intravenously before hemorrhagic shock in glutathione (GSH) group (n=8). Shock was induced with bleeding and mean arterial pressure was maintained 50 mmHg for 30 minutes. Recovery from shock was done with transfusion of preserved blood and maintained for 30 minutes. We measured arterial ketone bodies and ketone body ratio before, during and after shock, and compared them to control group (n=8) which was not pretreated with glutathione. AKBR during and after hemorrhagic shock in GSH group (0.8 and 1.0) were higher than those in control group (0.5 and 0.8). Light microscopic examination of liver biopsy revealed less portal degeneration during and after hemorrhagic shock in GSH group than control group. Pharmacologic modulation of hepatocytic function with glutathione before hemorrhagic shock has shown some beneficial effect with protection of decreased AKBR and histological change during and after hemorrhagic shock.