Teng C M, Jy W, Ouyang C
Toxicon. 1984;22(3):463-70. doi: 10.1016/0041-0101(84)90090-4.
Cardiotoxin, isolated from Naja naja atra snake venom, potentiates platelet aggregation induced by ADP, thrombin, collagen and venom phospholipase A2. The malondialdehyde formation caused by ADP, thrombin and venom phospholipase A2 were also increased in the presence of cardiotoxin. Both potentiation of aggregation and increase in malondialdehyde were blocked by indomethacin or Ca2+ (5 mM or 0.05 mM). Cardiotoxin did not potentiate thrombin-induced aggregation of p-bromophenacyl bromide-modified platelets. Thromboxane B2 formation induced by thrombin or collagen was also increased by cardiotoxin, while that by arachidonate was not affected. As a membrane-active polypeptide, cardiotoxin might augment the Ca2+-flux during the activation of the platelet membrane by aggregation inducers and then increase the activation of endogenous phospholipase A2.
从眼镜蛇蛇毒中分离出的心脏毒素可增强由二磷酸腺苷（ADP）、凝血酶、胶原蛋白和蛇毒磷脂酶A2诱导的血小板聚集。在存在心脏毒素的情况下，由ADP、凝血酶和蛇毒磷脂酶A2引起的丙二醛形成也会增加。吲哚美辛或钙离子（5 mM或0.05 mM）可阻断聚集增强和丙二醛增加。心脏毒素不会增强凝血酶诱导的对溴苯甲酰溴修饰血小板的聚集。心脏毒素还会增加由凝血酶或胶原蛋白诱导的血栓素B2形成，而对花生四烯酸诱导的血栓素B2形成没有影响。作为一种膜活性多肽，心脏毒素可能在聚集诱导剂激活血小板膜的过程中增加钙离子通量，进而增加内源性磷脂酶A2的激活。
