Liu G S
Department of Cardiology, Chinese PLA General Hospital, Military Postgraduate Medical School, Beijing.
Zhonghua Bing Li Xue Za Zhi. 1994 Apr;23(2):115-7.
The ultrastructural degenerative changes and calcium ion distribution observed in the rabbit myocardium after various periods of ischemia and 30 minutes after postischemia reperfusion after 30 minutes reperfusion following 15 minutes of ischemia, near complete recovery of substructures is seen, anyhow the number of calcium ion deposits along the sarcolemma are still lower than normal. After 30 and 45 minutes of ischemia, severe degenerative changes in various cellular substructures took place. The sarcolemma of most myocytes became devoid of precipitate. After reperfusion, large calcium ion deposits accumulated in the form of clusters in the mitochondria. It was recognized that the herein described cytochemical calcium ion shifts may be indicative of structural damage bordering irreversibility. After 60 to 75 minutes of ischemia and then postischemia reperfusion, cell damage is observed as disrupted sarcolemma completely devoid of calcium ion deposit, large swollen mitochondria without signs of calcium ions and presence of flocculent precipitates, all signs of terminal impairment of metabolism.
在兔心肌缺血不同时间段后以及缺血15分钟后再灌注30分钟、缺血后再灌注30分钟后观察到超微结构退行性变化和钙离子分布情况。可见亚结构几乎完全恢复,然而沿肌膜的钙离子沉积数量仍低于正常水平。缺血30分钟和45分钟后,各种细胞亚结构发生严重退行性变化。大多数心肌细胞的肌膜无沉淀物。再灌注后,大量钙离子以簇状形式聚集在线粒体中。据认为,本文所述的细胞化学钙离子移位可能表明结构损伤接近不可逆性。缺血60至75分钟后再进行缺血后再灌注,观察到细胞损伤,表现为肌膜破裂且完全无钙离子沉积、线粒体肿大且无钙离子迹象以及出现絮状沉淀物,所有这些都是代谢终末受损的迹象。