Abstract
Free fatty acids, which increase during brain ischemia, exert profound effects on the subsequent brain cell injury, and calcium (Ca2+) is considered to be involved in the production of these free fatty acids. On the other hand, binding assays or autoradioagraphic studies have established the presence of dihydropyridine (DHP) binding sites in the brain tissue. In this study, we examined the effects of YC-170, a synthetized Ca2+ agonist, on the liberation of free fatty acids in the ischemic rat brain using the decapitation model. The results show that the YC-170 accelerates the liberation of free fatty acids significantly. These findings seem to indicate that the Ca2+ influx via the DHP sensitive channel influences cerebral phospholipid metabolism during ischemia, and also seem to provide supportive evidence of the protective effects of the DHPs against ischemic cell injury on the brain.
