Both animal models of experimental myocardial infarction and clinical studies on reperfusion therapy for acute myocardial infarction have provided evidence of impaired tissue perfusion at the microvascular level after initiation of reperfusion despite adequate restoration of epicardial vessel patency. Characteristics of this "no-reflow" phenomenon found in basic science investigations, such as distinct perfusion defects, progressive decrease of resting myocardial flow with ongoing reperfusion and functional vascular alterations are paralleled by clinical observations demonstrating similar features during the course of reperfusion. In experimental animal investigations of coronary occlusion and reperfusion, this no-reflow phenomenon could be characterized as a fundamental mechanism of myocardial ischemia and reperfusion. Major determinants of the amount of no-reflow are the duration of occlusion, infarct size, but also the length of reperfusion, as rapid expansion of perfusion defects occurs during reperfusion. Moreover, no-reflow appears to persist over a period of at least four weeks, a period when major steps of infarct healing take place. The significant association of the degree of compromised tissue perfusion at four weeks and indices of infarct expansion, found in chronic animal models of reperfused myocardial infarction, might be the pathoanatomic correlate for the prognostic significance observed in the clinical setting.

译文

实验性心肌梗死的动物模型和急性心肌梗死再灌注治疗的临床研究都提供了尽管心外膜血管通畅性得到充分恢复,但再灌注开始后微血管水平组织灌注受损的证据。在基础科学研究中发现的这种 “无复流” 现象的特征,例如明显的灌注缺陷,静息心肌血流的进行性减少和持续的再灌注以及功能性血管改变,与临床观察结果平行,证明了在再灌注过程中的相似特征。在冠状动脉闭塞和再灌注的实验动物研究中,这种无复流现象可以表征为心肌缺血和再灌注的基本机制。无回流量的主要决定因素是闭塞的持续时间,梗塞面积以及再灌注的长度,因为在再灌注过程中会发生灌注缺陷的快速扩展。此外,无复流似乎持续了至少四个星期,这是发生梗塞愈合的主要步骤。在再灌注心肌梗塞的慢性动物模型中发现,在四周时组织灌注受损程度与梗塞扩展指数之间的显着关联,可能是在临床环境中观察到的预后意义的病理解剖相关。

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