PLATELET-ACTIVATING-FACTOR IS AN IMPORTANT MEDIATOR IN HYPOXIC-ISCHEMIC BRAIN INJURY IN THE NEWBORN RAT

Hypoxic-ischemic encephalopathy is still a very important cause of neo natal mortality and morbidity. Recently, platelet-activating factor (P AF) has been accused of being responsible for the neuronal damage in h ypoxic-ischemic brain. We investigated tissue PAF concentrations in hy poxic-ischemic brain injury in immature rats. Endogenous PAF concentra tion in brain tissue showed a marked increase in hypoxic-ischemic pups (85.6 +/- 15.5 pg/mg protein) when compared to that of control (9.05 +/- 3.1 pg/mg protein). In addition, we examined the effects of flunar izine, a selective calcium channel blocker, and Ginkgo biloba extract (EGb 761) on endogenous PAF concentration in hypoxic-ischemic brain in jury. Endogenous PAF concentrations in both flunarizine-pretreated (16 .6 +/- 4.8 pg/mg protein) and EGb 761-pretreated (33.5 +/- 8.9 pg/mg p rotein) pups were significantly lower than the untreated group. These results indicate that PAF is an important mediator in immature rat mod el of cerebral hypoxic-ischemic injury. The suppressor effect of fluna rizine and EGb 761 on PAF production may open new insight into the tre atment of hypoxic-ischemic brain injury.