中文摘要：

目的：观察急性心肌梗死直接经皮冠状动脉腔内成形术（PTCA）再灌注治疗无复流患者局部冠状动脉循坏内皮细胞凋亡及凝血活性的改变，探讨无复流的形成机制。方法：收集急性心肌梗死直接PTCA再灌注治疗无复流8例及有复流患者10例，同时选取稳定型心绞痛行择期PTCA和单纯冠状动脉造影的患者作为对照。流式细胞术检测患者冠状静脉窦血液标本内皮细胞凋亡情况及组织因子、血管性血友病因子（vWF）活性的改变。结果：无复流组内皮细胞凋亡数、组织因子及vWF水平分别为（985±245）×10^3/L、（359±67）ng／L、（292±39）％，均显著高于有复流组[（228±81）×10^3/L、（209±74）ng／L、（192±35）％]及对照组（均P〈o．01）。结论：冠状动脉内皮细胞凋亡及高凝状态参与了急性心肌梗死无复流的发病，其机制可能与内皮细胞凋亡导致弥散性微血栓阻塞冠状动脉微循环有关。

英文摘要：

Objective：To explore the mechanism of no-reflow phenomena in myocardial infarction patients underwent direct PTCA, to determine whether coronary endothelial cell apoptosis and prethrombosis play a role in the pathogenesis of no-reflow. Method：Eight patients with no-reflow phenomena, 10 patents without no-reflow and other patients as control groups （stable angina underwent selective PTCA or single coronary angiography） were recruited in the study. The coronary venous sinus circulating endothelial cell apoptosis was detected by flow cytometry （CD146±cells that stained for Annexin V）. And the coronary sinus plasma tissue factor and yon Wille brand factor were assayed by ELISA kit. Result：Circulating endothelial cell apoptosis （985± 245eell/ml）, plasma tissue factor （359±67ng/L） and yon Willebrand factor （[292± 39]%） in no-relow group were higher than myocardial infarction without no-reflow group （apoptosis [228±81]ml, tissue factor [209±74]ng/L, and vWF E192±35] % ） and other 2 groups significantly respectively （ P 〈0. 01）. Conclusion： Local coronary endothelial cell apoptosis and prethrombosis play a role in the pathogenesis of no-reflow in myocardial infarction patients underwent direct PTCA, the mechanism perhaps is that micro-circulation was occluded by micro thromobi which induced by endothelial cell apoptosis and prethromobosis.