体外循环时抑肽酶保护血小板功能的机制

The Mechanism of Preserving Platelet Function by Aprotinin During Cardiopulmonary Bypass

目的：研究体外循环过程中抑肽酶保护血小板功能的机制。方法：检测指标有血小板α－颗粒膜蛋白１４０，溶酶体完整膜蛋白、质膜糖蛋白Ｉｂ、ＩＩｂ／ＩＩａ复合物。对象是择期瓣膜替换术患者３０例。对照组１０例；实验Ａ组（进口抑肽酶组２５×１０５单位）１０例；实验Ｂ组（国产抑肽酶组２５×１０５单位）１０例。肝素化１０分、体外循环４０分、体外循环结束及结束后１小时４个点对比观察。结果：α－颗粒膜蛋白１４０及溶酶体完整膜蛋白阳性血小板百分数实验组与对照组相比，有显著差异（Ｐ＜０．０１）；血小板质膜糖蛋白Ｉｂ平均荧光强度实验组与对照组相比，有显著差异（Ｐ＜０．０１）；质膜糖蛋白ＩＩｂ／ＩＩａ平均荧光强度实验组与对照组相比，无显著差异（Ｐ＞０．０５）；纵隔引流量显示用药组术后６、２４小时血液丢失量明显低于未用药组（Ｐ＜０．０１）。结论：抑肽酶通过保护血小板粘附受体和减少其活化而保护血小板功能，体外循环中使用它可有效地减少术后出血及输血并肯定了国产抑肽酶的药效。

Objective:To study the mechanism of aprotinin in preserving the platelet function during cardiopulmonary bypass. Methods:Thirty patients with heart valvular prosthesis were randomized into three groups.10 patients (group A)received imported aprotinin (25×10 5 IU),10(group B)domestic aprotinin (25×10 5 IU)in pump prime, and 10(group C)controls.Platelet membrane glycoproteins (GP Ib, GP IIb/IIIa,GMP 140,LIMP CD63) were determined by immunofluorescence using flow cytometry(FCM)during cardiopulmonary bypass(CPB). Results:There were significant increase in GMP 140,LIMP CD63( p <0 01)and decrease in GPIb( p <0 01) in the aprotinin groups (A,B)during CPB vs.the control group;there were no significant difference in the GP IIb/IIIa( p >0 05);cumulative blood loss 6 h and 24 h after chest closure was significantly less in the aprotinin groups ( p <0 01). Conclusion:Aprotinin preserves the platelet function by decreasing platelet membrane GP Ib loss and inhibiting platelet activation and thus decreases postoperative blood loss effectively.Domestic aprotinin is equally effective as imported aprotinin. [WT5”HZ〗