血小板膜糖蛋白Ⅱb/Ⅲa受体激活在再灌注心肌无复流形成中的作用

Role of platelet membrane glycoprotein Ⅱb/ Ⅲa receptor activation in no-reflow after my - ocardial reperfusion

目的探讨血小板激活的表面标志物糖蛋白(GP)Ⅱb/Ⅲa受体活性在心肌再灌注无复流形成前后的改变,为心肌无复流的治疗提供指导。方法利用成年杂种犬的缺血再灌注模型,用心肌声学造影判断心肌无复流的造型,采用酶联免疫分析法测定心肌缺血3 h后再灌注以前和3 h再灌注以后,有复流与无复流心肌的外周静脉血(PVB)和冠状窦静脉血(SVB)血小板GPⅡb/Ⅲa受体活性。结果心肌缺血后再灌注以前PVB和SVB中的GPⅡb/Ⅲa受体活性均明显增高(P<0.001),提示血小板激活;3 h再灌注后心肌有复流和无复流组SVB中GPⅡb/Ⅲa受体活性均有明显的降低(P<0.001),心肌无复流组受体活性下降的更加显著(P<0.01),说明心肌微循环内发生了血小板受体的消耗,意味着有血小板的聚集。结论心肌缺血可以激活血小板,缺血和再灌注损伤可以使心肌微循环内发生血小板的粘附聚集,这与再灌注无复流的发生有密切的关系,很可能是其发生机制之一。

Objective To observe the changes in the activity of platelet glycoprotein (GP) Ⅱb/Ⅲa receptor following the oc-currence of no-reflow after myocardial reperfusion, to explore the measures for clinical management of this condition. Meth-ods Nine canine models of no-reflow following myocardial ischemia verified by reperfusion myocardial contrast echocardiog-raphy were used in this investigation. The peripheral venous blood (PVB) and sinus venous blood (SVB) were sampled before myocardial reperfusion (after a 3-hour myocardial ischemia) and after a 3-hour reperfusion for determinating GP Ⅱb/Ⅲa re-ceptor activities by means of enzyme-linked immunosorbent assay (ELISA). Results The activity of platelet GP Ⅱb/Ⅲa of PVB, either in 3-hour ischemic group or in 3-hour reperfusion group, was elevated significantly (P<0.001), suggesting platelet activation. Elevated platelet GP Ⅱb/Ⅲa receptor activity in SVB occurred only in 3-hour ischemic group, and the 3-hour reperfusion group (P<0.001) and the no-reflow group had significantly decreased activities, which was more obvious in the latter group (P<0.01). The findings signified the consumption of the platelet GP Ⅱb/Ⅲa receptors in the myocardial microcir-culation and the presence of platelet aggregation. Conclusions Myocardial ischemia may activate the platelets to express GP Ⅱb/Ⅲa receptors through stress response mechanism and damage the endothelia of the microvasculature to incur adhesion and aggregation of the platelets within the microcirculation, which may be one of the pathogeneses for myocardial no-reflow phenomenon.