抑肽酶对犬体外循环过程中血小板保护作用的实验研究

Study of the preserving effect of aprotinin on canine platelet during cardiopulmonary bypass

目的 探讨体外循环 (CPB)心脏手术中大剂量抑肽酶保护血小板的作用及机制。方法 实验犬随机分组 ,实验组给予大剂量抑肽酶 ,对照组给予等量生理盐水。检测血小板计数、血小板聚集率、血浆血栓烷B2 、血小板活化标记蛋白 - 140分子数、血小板膜糖蛋白Ib。结果大剂量抑肽酶可降低CPB过程中血浆血栓烷B2 含量和血小板活化标记蛋白 - 140分子数 ,保护血小板膜糖蛋白Ib ,但不影响血小板计数和ADP诱导的血小板聚集率。结论大剂量抑肽酶可能从以下两方面保护血小板功能 :(1)抑制纤维蛋白溶解酶 ,保护血小板膜糖蛋白Ib ,保护血小板粘附功能。 (2 )抑制血小板内花生四烯酸转化为血栓烷A2 ,减少血小板活化 ,从而保护血小板结构及功能的完整性。

Objective To investigate the effect of aprotinin on preserving platelet and the mechanism that high dose of aprotinin may prevent platelet function during cardiopulmonary bypass Methods Ten dogs were randomized into 2 groups (AP group and C group) before surgery In the AP group, each dog received high dose of aprotinin; in the C group, the same volume of saline was administered Serial blood samples were collected during and after cardiopulmonary bypass in both groups and platelet function was evaluated by examining platelet count (PTC), maximum platelet aggregation induced by ADP(Pagg), plasma thromboxane B2(TXB2),α-granule membrane protein-140 on the surface of platelet (GMP-140) and glycoprotein Ib(GPIb) Results Administration of high dose of aprotinin during cardiopulmonary bypass neither affected platelet count nor improved the maximum aggregation induced by ADP while TXB2 and GMP-140 on the surface of platelet was suppressed, and platelet GPIb was preserved Conclusion s It appears that the mechanism of aprotinin to preserve platelet during cardiopulmonary bypass may be interpreted in different ways:(1) Aprotinin treatment suppresses plasmin and preserves platelet glycoprotein Ib thereby protects platelet adhesive capacity during CPB (2) Aprotinin treatment suppresses the conversion of arachidonic acid into TXA2, reduces platelet activation and preserves platelet function