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
asa result of hepatic ischemia and following reperfusion. Arterial ketone body ratio(AKBR) is adequate 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 E1on 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 PCE1 continuously from 10 min before clamp to 30 min after declamp in PGE group, AKBR and hepatic histological findings before 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 AKBR 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 microscopic 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.
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