Effect of transient ischemia on free fatty acids and phospholipids in the gerbil brain

Abstract

The effect of transient bilateral carotid occlusion on levels of free fatty acids, phospholipids and lipid peroxides in the brain was studied in gerbils. During occlusion, saturated and polyunsaturated free fatty acids increased to .apprx. 11 fold in 30 min. During recirculation, a selectively rapid decrement occurred in arachidonic acid; saturated fatty acids gradually decreased to their basal levels in 180 min. The peroxide level, estimated by a thiobarbituric acid test, did not change during occlusion but was elevated on reperfusion. Phosphatidylethanolamine content decreased throughout the periods examined. These results do not support a hypothesis that lipid peroxidation is initiated during ischemia by the lack of O2 at the terminus of the mitochondrial respiratory chain. It is suggested that severe cerebral ischemia disintegrates membrane phospholipids, probably through activation of hydrolytic enzymes, and that overt perioxidative processes take place during reflow by restoration of O2 supply. The peroxidative reactions may cause additional damage during the postischemic phase.