The interruption of hepatic blood flow has been adopted as a method of bleeding control in hepatectomy and liver transplantation. But this occlusion of hepatic inflow may result in significant hepatic injury by various kinds of oxygen radicals produced as a result of hepatic ischemia and following reperfusion. Arterial ketone body ratio(AKBR) is adequatc and convenient parameter by which both acute and prolonged changes of the hepatic function can be estimated. Pharmacological modulation of hepatic injury during warm ischemia and early reperfusion has shown some benefical effects. The authors conducted an experiment to evaluate the inhibitory effect of glutathione and prostaglandin E on hepatic injury due to acute hepatic ischemia and reperfusion. Thirty rabbits were divided into three groups, such as control(n=10), GSH(n=10) and PGE(n=10) groups. Acute hepatic ischemia was induced through the application of portal triad cross-clamping for 30 minutes, and thereafter hepatic reperfusion was induced with the removal of cross-clamping. A single bolus of 200 mg glutathione was injected 10 min before clamp in GSH group, and 200 ng/kg/min of PGE continuously from 10 min before clamp to 30 min after declamp in PGE group. AKBR and hepatic histological findings hefore clamp, 30 min after clamp, 5 min and 30 min after declamp, respectively were compared among 3 groups AKBR was markedly decreased during the clamping period in all groups (P<0.05). In control and PGE groups AKRR was significantly increased after reperfusion than before clamp (P<0.05), but was significantly lower than before clamp. Thirty minutes after reperfusion in GSH group AKBR returned to normal level and was significantly higher than in control group (P<0.05). On light tnicroscopic examination of liver biopsy, mild swollen hepatocytes in the centrilobular zone were seen at ischemia and reperfusion in control and GSH groups, but nearly normal hepatic architectures in PGE group. These results suggest that glutathione has some benefical effect on protection of hepatic dysfunction, and PGE1 on protection of hepatocellular injury during hepatic ischemia and reperfusion.