心肌缺血时血小板功能变化的机制(英文)

Mechanism of changes in platelet function during myocardial ischemia

研究了冠心病人以及实验大鼠心肌缺血期间血小板功能变化的机制。利用血小板聚集仪检测血小板聚集率 (PAgR)。应用CD41,CD6 2和标记第二抗体FITC在流式细胞仪上检查了GPⅡb/Ⅲa和GMP 140表达的变化。利用荧光血小板聚集仪测定了血小板ATP的释放量 ;利用血小板离子钙聚集仪检测胞浆内钙含量。结果表明缺血时PAgR的增高是由于血小板表面的GPⅡb/Ⅲa受体表达增加所致。缺血期间GMP - 140表达的增加表明心肌缺血时血小板易于被激活 ,并且黏滞性增高。心肌缺血时ATP释放量也明显增加。在血小板ATP释放反应和血小板聚集率之间有正反馈相互作用关系。心肌缺血能显著引起胞浆内钙含量的增高 ,后者是导致血小板功能异常变化的重要细胞内机制。

The mechanisms responsible for the changes of platelet function during myocardial ischemia were studied in patients with coronary heart disease and experimental rats. The platelet aggregation rate (PagR) was determined using aggregometer. With the use of CD41, CD62 and the labeled second antibody FITC, the changes of expression of GPⅡb/Ⅲa and GMP 140 were determined by flow cytometry. The release of ATP was measured by platelet fluorescent aggregometer. The platelet cytoplasmic Ca 2+ content was monitored using platelet ionized calcium aggregometer. It was shown that the increased PAgR during myocardial ischemia was resulted from the increasing expression of GPⅡb/Ⅲa receptor on the surface of platelet. The increased expression of GMP 140 during myocardial ischemia indicates that platelet is likely to be activated by myocardial ischemia and increase its adhesiveness. The platelet ATP releasing response was greatly enhanced during myocardial ischemia. There are positive feedback interactions between platelet releasing response and platelet aggregating response. The myocardial ischemia can induce a significant increase of cytoplasmic ionized calcium which is an important intracellular mechanism leading to various functional changes during myocardial ischemia.