Gasser R N, Dienstl F, Puschendorf B, Hauptlorenz S, Moll M, Dworzak E
Angiology. 1986 Dec;37(12 Pt 1):880-7.
Research during the last ten years into the pathophysiology of acute myocardial infarction (AMI) has made it gradually clearer that this is a phasic event. A number of independent authors have made this conclusion quite obvious. The authors of this review suggest that the alternating sequence of coronary spasm and dilatation should be described as the "thromboischemic reentry mechanism," which itself leads to waves of reperfusion, producing characteristic episodic changes in some of the parameters of AMI. The spasms are brought about by substances let loose from aggregating platelets. Metabolites released during the concomitant ischemia lead the vessel from spasm to dilatation. Following thrombolytic treatment, the 'staccato' signs of myoglobinemia disappear, because of the withdrawal of the spasmogenic products of the platelets. It could also be shown that the concentration of myoglobin in the serum as a result of the dilating effect of calcium antagonists is twice the mean maximum value that the myoglobin time curve would show without such treatment.
过去十年对急性心肌梗死（AMI）病理生理学的研究逐渐明确这是一个阶段性事件。许多独立作者已使这一结论相当明显。本综述的作者认为，冠状动脉痉挛和扩张的交替序列应被描述为“血栓缺血再入机制”，其本身会导致再灌注波，在AMI的一些参数中产生特征性的间歇性变化。痉挛是由聚集的血小板释放的物质引起的。伴随缺血期间释放的代谢产物使血管从痉挛转为扩张。溶栓治疗后，肌红蛋白尿的“断奏”体征消失，这是因为血小板的痉挛原性产物减少。还可以表明，由于钙拮抗剂的扩张作用，血清中肌红蛋白的浓度是未进行此类治疗时肌红蛋白时间曲线所显示的平均最大值的两倍。
