The involvement of lipid peroxidation in renal
ischemia/reperfusion was explored by measuring changes in the cortical content of specific primary
lipid hydroperoxides (using chemluminescent detection with HPLC) following
ischemia and reperfusion and by correlating the changes in
hydroperoxide content with measurements of renal blood flow.
Phosphatidylcholine and
phosphatidylethanolamine hydroperoxide concentrations were significantly lowered during 30 or 60 min of
ischemia (to levels less than 50% of control at 60 min). Following 30 min of renal
ischemia, reperfusion resulted in a rebound of
phospholipid hydroperoxide tissue content to levels higher than controls. Increased
phospholipid hydroperoxide formation was not, however, observed in response to reperfusion following long-term (60 min)
ischemia. In separate animals it was demonstrated that following 30 min
ischemia and reperfusion, renal blood flow recovers to about 65% of control in 1 h. In contrast, following 60 min
ischemia and reperfusion, the renal blood flow remains more highly impaired (less than 25% recovery for periods up to 24 h). These results imply that
phospholipid hydroperoxides are produced and accumulate in the kidneys under normal aerobic conditions and that
lipid peroxidative activity increases during renal
ischemia/reperfusion to an extent dependent on the degree of local blood perfusion.