医学
心肌梗塞
细胞凋亡
心肌保护
坏死
溶栓
心脏病学
DNA断裂
程序性细胞死亡
碎片(计算)
琼脂糖凝胶电泳
缺血
内科学
心肌细胞
梗塞
尸检
病理
DNA
生物
生物化学
生态学
作者
Antti Saraste,Kari Pulkki,Markku Kallajoki,K Henriksén,Martti Parvinen,Liisa‐Maria Voipio‐Pulkki
出处
期刊:Circulation
[Ovid Technologies (Wolters Kluwer)]
日期:1997-01-21
卷期号:95 (2): 320-323
被引量:810
标识
DOI:10.1161/01.cir.95.2.320
摘要
Background After reopening of the infarct-related coronary artery, cardiomyocytes continue to die during reperfusion. The mechanisms of cell death have been subject to debate. We studied whether an apoptotic type of cell death occurs in human acute myocardial infarction (AMI). Methods and Results We studied myocardial samples of eight patients who died of AMI and had patent infarct-related arteries at autopsy. Six of the patients had received initially successful thrombolysis. Extensive formation of DNA strand breaks, the typical biochemical feature of apoptosis, was detected with the use of the in situ DNA end-labeling method. Apoptotic cardiomyocytes were observed particularly in the border zones of histologically infarcted myocardium, whereas very few apoptotic cells were present in the remote noninfarcted myocardium. Internucleosomal fragmentation was confirmed by agarose gel electrophoresis of DNA isolated from the representative myocardial areas. Conclusions This study provides evidence that in addition to overt necrosis, a subset of myocytes undergo apoptosis during ischemia-reperfusion injury. Apoptosis may provide a new target for cardioprotection during evolving AMI in humans.
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