Early phase of myocardial ischemic injury and infarction.
Early phase of myocardial ischemic injury and infarction.
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心肌缺血损伤和梗塞的早期阶段。
DOI：
10.1016/0002-9149(69)90464-0
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发表时间：
1969
期刊：
影响因子：
--
通讯作者：
R. Jennings
中科院分区：
文献类型：
--
作者：
R. Jennings
本文综述了缺血对心肌组织的急性影响，着重介绍了犬实验性心肌缺血损伤中观察到的事件与急性心肌梗死后最初几小时内人心肌的动态变化之间的关系。缺血对心肌的一般影响包括局部氧气和代谢物等物质供应减少所致的继发性影响，以及由于乳酸和电解质等物质从血流不良的缺血组织扩散到全身循环而造成的变化。细胞死亡(不可逆性损伤)首先发生在犬心脏最大损伤区域的缺血20分钟后，而梗塞在闭塞后60至120分钟内尚未完全形成。在细胞死亡发生之前，严重的缺血细胞受到可逆性的损伤，并表现出与正常细胞不同的变化。这些变化包括糖原和高能磷酸盐供应的枯竭，乳酸和氢含量的增加，肌原纤维的松弛和收缩的失败。刚刚死亡的细胞表现出与线粒体、电解质和核缺陷相同的变化。如果有上述变化，是否会导致缺血性损伤中的不可逆性发展仍有待确定。提供的一些数据支持线粒体缺陷可能在不可逆状态的发生中起关键作用的假设。
The acute effects of ischemia on myocardial tissue are reviewed in this paper with emphasis on how the events observed in experimental myocardial ischemic injury in dogs relate to the sequential changes occurring in the myocardium of man during the first few hours after the onset of acute infarction. The general effects of ischemia on myocardium include those which are secondary to a diminished local supply of substances such as oxygen and metabolites as well as changes resulting from the impaired diffusion of substances such as lactic acid and electrolytes from the poorly perfused ischemic tissue to the general circulation. Cell death (irreversible injury) first develops after 20 minutes of ischemia in areas of maximum injury in the dog heart and infarcts are not fully developed for 60 to 120 minutes after occlusion. Prior to the development of cell death, the severely ischemic cells are reversibly injured and show a variety of alterations from normal. These changes include depletion of supplies of glycogen and high energy phosphate, increased content of lactic acid and hydrogen, relaxation of myofibrils and failure of contraction. Cells which have just died show the same changes as well as mitochondrial, electrolyte, and nuclear defects. Which, if any, of the preceding changes causes the development of irreversibility in ischemic injury remains to be established. Some data is presented in support of the hypothesis that mitochondrial defects may be critical in the genesis of the irreversible state.