Effect of transient ischemia on free fatty acids and phospholipids in the gerbil brain. Lipid peroxidation as a possible cause of postischemic injury.

The effect of transient bilateral carotid occulsion on levels of free fatty acids, phospholipids, and lipid peroxides in the brain was studied in gerbils. During occulsion, both saturated and polyunsaturated free fatty acids increased strikingly to approximately 11-fold in total by 30 minutes. During recirculation, however, a selectively rapid decrement occurred in arachidonic acid, while saturated fatty acids gradually decreased to their basal levels in 180 minutes. 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 initated during ischemia by the lack of oxygen at the terminus of the mitochondrial respiratory chain. Instead, it is suggested that severe cerebral ischemia disintegrates membrane phospholipids, probably through activation of hydrolytic enzymes, and that overt peroxidative processes take place during reflow by means of restoration of oxygen supply. The peroxidative reactions may indeed, cause additional damage during the postischemic phase.