Rat liver postischemic lipid peroxidation and vasoconstriction depend on 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 enhanced generation of reactive oxygen species in a crystalloid perfused rat liver model. To evaluate the effect of reactive oxygen species generation upon the development of the postischemic hypoperfusion, hepatic vascular resistance was simultaneously monitored. One hour of ischemia did not produce sustained reactive oxygen species generation or development of no-reflow. Two hours of ischemia did not result in sustained reactive oxygen species generation but did produce no-reflow. Sustained 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 of ischemia is the threshold for sustained lipid peroxidation. Both lipid peroxidation and no-reflow could be mitigated through the administration of superoxide dismutase. Superoxide dismutase could reduce the amount of cell injury due to the enhanced lipid peroxidation induced by 2.5 h of ischemia. Limitation of reactive oxygen species generation to a critical threshold, either by restricting the duration of ischemia or by pharmacological intervention, may be an important means of preventing further cellular injury through no-reflow and lipid peroxidation.