抄録
Human umbilical vein endothelial cells (EC) in culture were exposed to hypoxiareoxygenation. Superoxide generation in EC was observed quickly after reoxygenation almost within one minute and this was inhibited by allopurinol. In the same experiments, EC injury and neutrophil adherence to EC were measured. EC injury after reoxygenation was detected by both 51Cr release and cell detachment methods. EC injury was more easily detected by cell detachment method and significantly enhanced by the presence of neutrophils, which was inhibited by allopurinol. Neutrophil adherence to reoxygenated, but not to normal or hypoxic EC was, again, significantly reduced by allopurinol treatment of EC.
These results indicate that superoxide which was produced in reoxygenated EC mediates enhanced neutrophil adherence to EC and EC injury following reoxygenation. Through these mechanisms, superoxide would play an important role in the formation of reperfusion injury besides the possible direct toxic effect to the reperfused tissues.
