摘要
观察了３３只家兔心肌不同缺血时间，再灌注３０ｍｉｎ后，心肌超微结构改变及Ｃａ￣（２＋）分布特点。缺血１５ｍｉｎ再灌注后，心肌结构接近正常，但肌纤维膜上Ｃａ￣（２＋）分布数量却低于正常心肌。缺血３０～４５ｍｉｎ，亚细胞结构发生了严重变性，大多数细胞肌纤维膜上Ｃａ￣（２＋）消失。再灌注后大量Ｃａ￣（２＋）以丛状形式沉积干线粒体内，称为不可逆损伤的边缘。缺血６０和７５ｍｉｎ与再灌注后，可见肌纤维膜断裂并完全失去了Ｃａ￣（２＋）的沉积。大而肿胀的线粒体内亦无Ｃａ￣（２＋）踪迹，代之以云絮状物质沉淀等细胞损伤、代谢的终未阶段征象。
he ultrastructural degenerative changes andcalcium ion distribution observed in the rabbit myocardium after various periods of ischemia and 30 minutes after postischemia reprefusion. after 30 minutes reperfusion following 15 minutes of ischemia, near complete recoverv of substructures is seen,anyhow the number of calcium ion deposites along the sarcolemma are still lower than noimal.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 forn1 of clusters in the mitochondria.It was recognized that the herein described cytochemical calcium ion shifts may be indicative of strtlctural damage bordering irreversibility.After 60 to 75 minutes of ischemia and then postischemia reperfusion, cell damage is observed as dis-rupted sarcolemma completely devoid of calcium ion deposit, large swollen mitochondria without signs of calcium ions and presence of flocculent precipitates,all signs of terminal impainnent of metabolism.
出处
《中华病理学杂志》
CAS
CSCD
北大核心
1994年第2期115-117,T026,共4页
Chinese Journal of Pathology
