血小板膜糖蛋白Ⅰa基因多态性在不稳定性心绞痛发生机制中作用的探讨

被引：3

作者：

王燕妮

赵永辉

祝家庆

马爱群

机构：

[1] 西安交通大学第一医院心内科

[2] 河南医科大学第二附属医院心内科

[3] 西安交通大学第一医院心内科陕西省西安市

来源：

中国循环杂志 | 2002年 / 02期

关键词：

心绞痛; 不稳定型; 基因; 糖蛋白; 多态性;

D O I：

暂无

中图分类号：

R541.4 [冠状动脉（粥样）硬化性心脏病（冠心病）];

学科分类号：

1002 ; 100201 ;

摘要：

目的 :探讨血小板膜糖蛋白 (GP)Ⅰa基因 80 7C/T多态性在不稳定性心绞痛 (UAP)发病机制中的作用。方法 :①体外应用Ⅰ型胶原诱导 ,观察 35例UAP(UAP组 )患者和 33例正常人 (正常对照组 )血小板聚集功能的变化 ;②用酶联免疫双抗体夹心法测定上述人群中血浆α颗粒膜蛋白 (GMP) 14 0浓度 ;③应用聚合酶联扩增实验 (PCR SSP)对上述人群进行血小板膜GPⅠa基因 80 7C/T多态性检测。结果 :①UAP患者和正常人TC基因型体外胶原诱导下血小板达 30 %聚集率前的迟缓期较CC基因型均显著缩短(P <0 0 5 ) ,但二者的最大血小板聚集率无显著性差异。UAP组与正常对照组对比 ,同基因型相比血小板达 30 %聚集前的迟缓期明显缩短 (P <0 0 1) ,最大血小板聚集率无显著差异。②UAP患者TC基因型血浆GMP 14 0浓度明显高于CC基因型 (P <0 0 5 ) ,与正常对照组同基因型比较亦有显著差异 (P <0 0 1)。③UAP组GPⅠa基因 80 7C/T中TC基因型比例 ( 5 7 14 % )大于正常对照组 ,但统计学无显著性差异。结论 :与血小板膜GPⅠa基因T80 7等位基因相关的胶原诱导下血小板聚集功能的迅速启动 ,可能为UAP发病的机制之一。

引用

页码：45 / 47

页数：3

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