Degradation of phospholipid molecular species during experimental cerebral ischemia in rats.

Previous investigators have shown that free fatty acids that accumulate during ischemia are an indicator of evolution in ischemic brain damage. Our study describes the temporal relations between free fatty acid accumulation and degradation of phospholipid molecular species after cerebral ischemia. Using the four-vessel occlusion model of adult Wistar rats, we analyzed quantitatively the cerebral phospholipid molecular species of diacyl phosphatidylcholine and diacyl phosphatidylethanolamine and released free fatty acids during ischemia. Total diacyl phosphatidylcholine molecular species decreased gradually but did not show any significant difference even at 60 minutes. By contrast, total diacyl phosphatidylethanolamine abruptly decreased after 5 minutes and continued to decrease significantly thereafter. Polyunsaturated molecular species showed a higher ratio of degradation than saturated and monounsaturated molecular species of either phosphatidylcholine or phosphatidylethanolamine. Total free fatty acid accumulated according to the time elapsed, and statistical significance was obtained after 10 minutes. Free arachidonic and docosahexaenoic acids were attributed to these significant accumulations at 10, 15, and 30 minutes. At 60 minutes, individual free fatty acids increased nonspecifically. Free fatty acids, which are hydrolyzed from phospholipid classes, are known to be further metabolized to bioactive substances such as prostaglandins and leukotrienes. Rapid degradation of phospholipid molecular species, especially of diacyl polyunsaturated molecular species, could be an important finding to membrane perturbation. Effective prevention of these changes might enhance tolerance to ischemic brain damage.