通常将心肌缺血后再灌注加重心肌损伤的现象称为再灌注损伤(retperluecointigury)。本文就冠脉阻塞后心肌缺血的发展过程,再灌注后缺血心肌的变化似及再灌注对缺血心肌损害的加重,白细胞对心肌细胞损害等方面进行论述。心肌梗塞时心肌的坏死过程心外膜下粗大的冠状动脉发生急性血运障碍,使该冠脉供血区心肌处于低灌流状态,因而发生心肌梗塞。结扎狗的冠状动脉主干,阻断冠脉血流,便该主干供血的心肌陷入缺血状态。但因缺血区尚可接受来自健侧侧支循环的血液供应,所以缺血状态并不均匀一致。Tennings 等人的研究表明:血流阻断40分钟以上,位于心内膜下的心肌首先发生不可逆变化。如不足15分钟则无细胞构造变化;此时若血流重新开放,可恢复心肌功能。但若超过20分钟以上,线粒体形态发生变化(肿大、内膜间隙增大),可出现含有嗜锇染色小颗粒的细胞。Tennings 等以这种线粒体的 Usually myocardial ischemia and reperfusion aggravate myocardial injury is called reperfusion injury (retperluecointigury). In this paper, the development of myocardial ischemia after coronary occlusion, changes in ischemic myocardium after reperfusion, as well as the reperfusion injury of myocardial ischemia increased, leukocyte damage to myocardial cells and so on. Myocardial infarction myocardial necrosis process Subepithelial coronary artery acute blood supply disorder, so that the coronary artery coronary artery in a low perfusion state, resulting in myocardial infarction. Ligation of the dog’s coronary artery trunk, blocking the coronary blood flow, then the trunk of myocardial infarction into the ischemic state. However, due to the ischemic area can still accept the blood supply from the contralateral collateral circulation, so the ischemic state is not uniform. Tennings et al study showed that: blood flow blocked for more than 40 minutes, located in the subendocardial myocardial irreversible change first. If less than 15 minutes no change in cell structure; at this time if the blood flow to reopen, can restore myocardial function. However, if more than 20 minutes or more, changes in the morphology of mitochondria (enlargement, increased intima-media gap), there may be osmiophilic staining of small particles of cells. Tennings and so on with this mitochondrial