REPERFUSION INJURY INDUCES APOPTOSIS IN RABBIT CARDIOMYOCYTES
REPERFUSION INJURY INDUCES APOPTOSIS IN RABBIT CARDIOMYOCYTES
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DOI：
10.1172/jci117504
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发表时间：
1994-10-01
影响因子：
15.9
通讯作者：
ENGLER, RL
中科院分区：
文献类型：
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作者：
GOTTLIEB, RA;BURLESON, KO;ENGLER, RL
限制心肌缺血性坏死最有效的方法是再灌注，但再灌注本身可能导致组织损伤，这一直难以与缺血性损伤分开。这份报告确定了细胞凋亡（程序性细胞死亡）在心肌细胞的再灌注反应，而不是缺血的元素。细胞凋亡的标志，核小体梯状DNA片段（约200个碱基对），在缺血/再灌注兔心肌组织中检测到，但在正常或缺血只兔心脏。粒细胞减少并不能阻止核小体DNA裂解。原位缺口末端标记显示DNA片段化主要发生在心肌细胞。透射电镜下，再灌注组的核染色质凝聚模式与持续缺血组明显不同。凋亡可能是心肌细胞再灌注损伤的一个特征，导致晚期细胞死亡。
The most effective way to limit myocardial ischemic necrosis is reperfusion, but reperfusion itself may result in tissue injury, which has been difficult to separate from ischemic injury. This report identifies elements of apoptosis (programmed cell death) in myocytes as a response to reperfusion but not ischemia. The hallmark of apoptosis, nucleosomal ladders of DNA fragments (approximate to 200 base pairs), was detected in ischemic/reperfused rabbit myocardial tissue but not in normal or ischemic-only rabbit hearts. Granulocytopenia did not prevent nucleosomal DNA cleavage. In situ nick end labeling demonstrated DNA fragmentation predominantly in myocytes. The pattern of nuclear chromatin condensation was distinctly different in reperfused than in persistently ischemic tissue by transmission electron microscopy. Apoptosis may be a specific feature of reperfusion injury in cardiac myocytes, leading to late cell death.