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本文测定了家兔红细胞裂解产物(EBP)和血小板对牛离体基底动脉的收缩效应,以探讨它们在蛛网膜下腔出血(SAH)后晚期脑血管痉挛(CVS)发病中的作用。结果表明,EBP 和血小板均有明显的缩血管效应;温育5—10天,EBP 的缩血管效应减弱而血小板的效应则有所增强;加热100℃10分钟,EBP 的缩血管作用消失,而血小板及标准对照物质5—HT、组胺和 NE 的缩血管作用不减弱;血小板的缩血管作用能被酚苄明阻断,且为阿斯匹林减弱;EBP 可诱导血小板聚集,促进其 TXA:合成。这些结果提示:EBP 和血小板在晚期 CVS 发病中都可能起重要作用,血小板的缩血管作用与血管活性(?)类物质和前列腺素类物质有关,EBP 则可能一方面直接引起 CVS,另一方面通过激活血小板而加重 CVS。
In this paper, the contractile effects of rabbit erythrocyte lysate (EBP) and platelets on bovine isolated basilar artery were measured in order to investigate their role in the pathogenesis of advanced cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH). The results showed that both EBP and platelets had obvious vasoconstrictor effect. After 5-10 days of incubation, the vasoconstrictor effect of EBP was weakened and the platelet effect was enhanced. The vasoconstriction of EBP disappeared when heated at 100 ° C for 10 minutes Platelet and standard reference substances 5-HT, histamine and NE vasoconstriction is not reduced; platelet vasoconstriction can be blocked by phenoxybenzamine and aspirin weakened; EBP can induce platelet aggregation and promote TXA :synthesis. These results suggest that both EBP and platelets may play an important role in the pathogenesis of advanced CVS. The vasoconstrictor effect of platelets is related to vasoactive substances and prostaglandins. EBP may cause CVS directly on the one hand, CVS is exacerbated by activating platelets.