Abstract
Flunarizine in vivo protects against endothelial cell damage induced by intravenous injection of citrate, CaCl2, or lactate in rats. Its effect is optimal at the low oral dose of 0.1 mg/kg, corresponding to the clinically used one. It lasts for at least 8 hours. Edema formation, platelet activation, and venostatic thrombosis subsequent to endothelial cell injury consequently are also in hibited by flunarizine. The compound does not affect platelet function, plasma coagulation or generation of PGI2 by vascular tissue and does not impair normal haemostasis at effective doses. As for its vascular and hemor rheological effects, the protection by flunarizine against endothelial injury may be related to its Ca2+-antagonistic properties.
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