Di Minno G, Shapiro S S, Catalano P M, De Marco L, Murphy S
Blood. 1983 Jul;62(1):186-90.
Following stimulation with arachidonic acid, collagen, U-46619 (a stable analogue of prostaglandin endoperoxide/thromboxane-A2), thrombin, or adenosine diphosphate (ADP), unstirred human platelet suspensions bound labeled factor VIII in a reaction that reached equilibrium within 10 min. Apyrase inhibited binding induced by arachidonic acid, collagen, U-46619, and thrombin by less than 40%, but inhibited ADP-induced binding by 95%. Binding to aspirin-treated platelets was normal in response to U-46619, reduced by 60%-70% in response to ADP, collagen, and thrombin, and absent in response to arachidonic acid. Binding in response to U-46619 was not altered by the combination of apyrase and aspirin. Binding of factor VIII was decreased by 90% when 10 mM EDTA was added before each agonist, but it was inhibited less than 30% when EDTA was added following platelet stimulation. We conclude that arachidonic acid, collagen, and thrombin can expose binding sites for factor VIII independently of released ADP; that Ca++ is required for activation but probably not for binding of factor VIII to platelets; and that platelet thromboxane synthesis plays a major role in the binding of factor VIII to platelets induced by thrombin, ADP, or collagen.
在用花生四烯酸、胶原蛋白、U - 46619（前列腺素内过氧化物/血栓素 - A2的稳定类似物）、凝血酶或二磷酸腺苷（ADP）刺激后，未搅拌的人血小板悬液在10分钟内达到平衡的反应中结合标记的因子VIII。腺苷三磷酸双磷酸酶抑制花生四烯酸、胶原蛋白、U - 46619和凝血酶诱导的结合不到40%，但抑制ADP诱导的结合达95%。对U - 46619的反应，阿司匹林处理的血小板结合正常；对ADP、胶原蛋白和凝血酶的反应，结合减少60% - 70%；对花生四烯酸的反应，结合不存在。对U - 46619的反应，腺苷三磷酸双磷酸酶和阿司匹林联合使用时结合未改变。在每种激动剂加入前加入10 mM乙二胺四乙酸（EDTA）时，因子VIII的结合减少90%，但在血小板刺激后加入EDTA时，抑制小于30%。我们得出结论：花生四烯酸、胶原蛋白和凝血酶可独立于释放的ADP暴露因子VIII的结合位点；Ca++是激活所必需的，但可能不是因子VIII与血小板结合所必需的；血小板血栓素合成在凝血酶、ADP或胶原蛋白诱导的因子VIII与血小板的结合中起主要作用。
