Reimer K A, Lowe J E, Rasmussen M M, Jennings R B
Circulation. 1977 Nov;56(5):786-94. doi: 10.1161/01.cir.56.5.786.
Irreversible ischemic myocardial cell injury developes in an increasing number of cells as the duration of coronary occlusion is prolonged. The present study quantitates myocardial necrosis produced by 40 minutes, 3 hours, or 6 hours of temporary circumflex coronary occlusion (CO) followed by 2 to 4 days of reperfusion, or by 24 or 96 hours of permanent circumflex ligation in pentobarbital anesthetized open chest dogs. After 40 minutes of ischemia, myocyte necrosis was subendocardial but with increasing duration of coronary occlusion, irreversible injury progressed as a wavefront toward the subepicardium. Transmural necrosis was 38 +/- 4% after 40 min, 57 +/- 7% after 3 hours, 71 +/- 7% after 6 hours and 85 +/- 2% after 24 hours of ischemic injury. These results document the presence of a subepicardial zone of ischemic but viable myocardium which is available for pharmacologic or surgical salvage for at least three and perhaps six hours following circumflex occlusion in the dog.
随着冠状动脉阻塞时间的延长，越来越多的细胞会发生不可逆的缺血性心肌细胞损伤。本研究对戊巴比妥麻醉的开胸犬进行了如下实验：临时回旋支冠状动脉阻塞（CO）40分钟、3小时或6小时，随后再灌注2至4天；或永久性结扎回旋支24小时或96小时，然后对产生的心肌坏死进行定量分析。缺血40分钟后，心肌细胞坏死位于心内膜下，但随着冠状动脉阻塞时间的延长，不可逆损伤呈波阵面向心外膜发展。缺血损伤40分钟后透壁坏死率为38±4%，3小时后为57±7%，6小时后为71±7%，24小时后为85±2%。这些结果证明，在犬冠状动脉回旋支阻塞后，至少三小时甚至六小时内，心外膜下存在缺血但仍存活的心肌区域，可通过药物或手术进行挽救。
