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为探讨蛛网膜下腔出血(SAH)后晚期脑血管痉挛(CVS)的发病机理,本文测定了兔红细胞裂解产物(EBP)和血小板对牛离体基底动脉的收缩效应。结果表明,EBP和血小板均有强烈的缩血管效应;温育5～10天后EBP的效应减弱而血小板的效应则有所增强;加热100℃10分钟,EBP的缩血管效应消失,而血小板及对照5—HT、组胺和NE的效应均不减弱;血小板的缩血管效应能被酚(艹卡)明阻断,为阿斯匹林减弱;EBP能诱导血小板聚集,促进其TXA_2合成。这些结果提示:EBP和血小板在晚期CVS发病中都可能有重要作用;血小板的缩血管效应与血管活性胺和前列腺素类物质有关;EBP一方面可直接引起血管收缩,另一方面则可能通过激活血小板而加重CVS。
In order to explore the pathogenesis of advanced cerebral vasospasm (CVS) after subarachnoid hemorrhage (SAH), the contractile effects of rabbit erythrocyte lysate (EBP) and platelets on bovine isolated basilar artery were measured. The results showed that both EBP and platelets had a strong vasoconstrictive effect. The effect of EBP was weakened and the platelet effect was enhanced after 5 to 10 days of incubation. The vasoconstriction of EBP disappeared after heating at 100 ° C for 10 minutes, while platelet and control 5-HT, histamine and NE are not weakened; vasoconstrictor effect of platelet can be blocked by phenol (acenaphthene), which is weakened by aspirin; EBP can induce platelet aggregation and promote TXA2 synthesis. These results suggest that both EBP and platelets may play an important role in the pathogenesis of advanced CVS. The platelet vasoconstriction is associated with vasoactive amines and prostaglandins. EBP can directly induce vasoconstriction on the one hand and activate Platelets aggravate CVS.