RAT-LIVER POSTISCHEMIC LIPID-PEROXIDATION AND VASOCONSTRICTION DEPENDON ISCHEMIA TIME

In this investigation, we used chemiluminescence to study the ability of increasing durations of ischemia (1, 2, or 2.5 h) to induce: enhanc ed generation of reactive oxygen species in a crystalloid perfused rat liver model. To evaluate the effect of reactive oxygen species genera tion upon the development of the postischemic hypoperfusion, hepatic v ascular resistance was simultaneously monitored. One hour of ischemia did not produce sustained reactive oxygen species generation or develo pment of no-reflow. Two hours of ischemia did not result in sustained reactive oxygen species generation but did produce no-reflow. Sustaine d reactive oxygen production was achieved after 2.5 h of ischemia and was accompanied by the development of no-reflow. We found that 2.5 h o f ischemia is the threshold for sustained lipid peroxidation. Both lip id peroxidation and no-reflow could be mitigated through the administr ation of superoxide dismutase. Superoxide dismutase could reduce the a mount of cell injury due to the enhanced lipid peroxidation induced by 2.5 h of ischemia. Limitation of reactive oxygen species generation t o a critical threshold, either by restricting the duration of ischemia or by pharmacological intervention, may be an important means of prev enting further cellular injury through no-reflow and lipid peroxidatio n. (C) 1998 Elsevier Science Inc.