Cellular damage of various organs by
ischemia following reperfusion is assumed to be at least in part due to lipid peroxidation in biomembranes, and
oxygen-derived
free radicals play a major role. The level of
lipid peroxides in liver tissue increased during 90-min
ischemia. When reflow of hepatic blood was allowed, a greater increase in the
lipid peroxides was observed. Similar increases were obtained in several
serum markers (GOT, GPT and LDH) during the period of
ischemia or
ischemia-reperfusion. In addition, levels of
cytochrome p-450 and
NADPH cyt. c
reductase activity decreased in proportion to the decrease in microsomal
proteins during
ischemia or
ischemia-reperfusion. On the other hand,
superoxide dismutase in blood was significantly increased by
ischemia-reperfusion. Rats died within 2 days after liver
ischemia of 90 min, while all animals subjected to 30-min
ischemia survived. Histopathological examinations indicated that extensive coagulation with erythrocytes occurred and the extent was dependent on the time of
ischemia. The liver injury by
ischemia-reperfusion could be a useful experimental model for studying liver injury induced by
free radicals, for developing hepatoprotective drugs, or for investigating
liver transplantation.