Huang T F, Yeh H I, Ouyang C
Toxicon. 1984;22(2):243-51. doi: 10.1016/0041-0101(84)90025-4.
The platelet aggregation inhibitor purified from Agkistrodon halys snake venom inhibited rabbit platelet aggregations induced by thrombin, sodium arachidonate, collagen or ionophore A-23187. The IC50 was about 11 micrograms/ml in platelet aggregation regardless of which aggregation inducer was used. beta-Mercaptoethanol abolished both the phospholipase A enzymatic and platelet aggregation inhibitory activities of this venom inhibitor. p-Bromophenacyl bromide-treated venom inhibitor lost almost completely its phosphilipase A enzymatic activity, but retained its platelet aggregation inhibitory effect. In the presence of EGTA, the venom inhibitor still showed the same inhibitory activity on thrombin-, sodium arachidonate-, collagen- or ionophore A23187-induced platelet aggregations triggered by successive addition of Ca2+. The activation of platelet phospholipase A and the serotonin release reaction triggered by Ca2+ influx were unaffected by this venom inhibitor. It also inhibited the clot retraction of platelet-rich plasma. It is concluded that the inhibitory effect of the venom inhibitor on platelet aggregation is independent of its phospholipase A enzymatic activity. Its mode of action is different from those of other known platelet inhibitory drugs. This venom inhibitor possibly acts on a common step subsequent to platelet shape change, leading to inhibition of platelet aggregation.
从蝮蛇蛇毒中纯化得到的血小板聚集抑制剂可抑制由凝血酶、花生四烯酸钠、胶原蛋白或离子载体A - 23187诱导的兔血小板聚集。无论使用哪种聚集诱导剂，在血小板聚集中其IC50约为11微克/毫升。β-巯基乙醇消除了这种蛇毒抑制剂的磷脂酶A酶活性和血小板聚集抑制活性。对溴苯甲酰溴处理的蛇毒抑制剂几乎完全丧失了其磷脂酶A酶活性，但仍保留其血小板聚集抑制作用。在乙二醇双四乙酸（EGTA）存在的情况下，该蛇毒抑制剂对连续添加Ca2 +引发的由凝血酶、花生四烯酸钠、胶原蛋白或离子载体A23187诱导的血小板聚集仍表现出相同的抑制活性。血小板磷脂酶A的激活以及由Ca2 +内流引发的5 -羟色胺释放反应不受该蛇毒抑制剂的影响。它还抑制富含血小板血浆的血块回缩。结论是，蛇毒抑制剂对血小板聚集的抑制作用与其磷脂酶A酶活性无关。其作用方式不同于其他已知的血小板抑制药物。这种蛇毒抑制剂可能作用于血小板形状改变后的一个共同步骤，从而导致血小板聚集的抑制。
