EFFECT OF REPERFUSION LATE IN THE PHASE OF REVERSIBLE ISCHEMIC-INJURY - CHANGES IN CELL-VOLUME, ELECTROLYTES, METABOLITES, AND ULTRASTRUCTURE
EFFECT OF REPERFUSION LATE IN THE PHASE OF REVERSIBLE ISCHEMIC-INJURY - CHANGES IN CELL-VOLUME, ELECTROLYTES, METABOLITES, AND ULTRASTRUCTURE
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DOI：
10.1161/01.res.56.2.262
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发表时间：
1985-01-01
影响因子：
20.1
通讯作者：
REIMER, KA
中科院分区：
文献类型：
--
作者：
JENNINGS, RB;SCHAPER, J;REIMER, KA
本文研究了在体心肌缺血15分钟后再灌注对可逆性损伤心肌的急性效应。分别于缺血15min末及复流0.5、0.3、20min后，观察心肌细胞腺苷酸池、细胞容积调节、心肌Ca及超微结构的变化。再灌注前，ATP和腺苷酸池分别减少了63%和44%的控制，腺苷酸电荷减少到0.65。再灌注3分钟后，腺苷酸电荷恢复到控制的腺苷单磷酸和二磷酸的再磷酸化，但ATP仍然减少了45%。在0.5分钟的再灌注后检测到轻度组织水肿，并持续20分钟的再灌注。组织H2O的增加伴随着Na的轻微增加和组织K的显著增加。虽然大量的钙积累发展时，不可逆损伤的组织再灌注，没有检测到钙超载可逆损伤的心肌细胞在早期再灌注。 再灌注3分钟加重了缺血15分钟引起的线粒体肿胀，但再灌注20分钟后，心肌超微结构基本正常，除了罕见的肿胀或破坏，线粒体。因此，可逆性损伤的肌细胞再灌注后，与短暂缺血相关的细胞异常持续不同的时间。虽然腺嘌呤核苷酸的补充非常缓慢，但腺苷酸电荷在3分钟后恢复，表明线粒体ATP生产迅速恢复。未检测到钙超载，但心肌水肿和增加钾持续整个20分钟的再灌注。缺血的超微结构的后果几乎逆转后20分钟的再灌注。
The acute effects of reperfusion on myocardium reversibly damaged by 15 min of severe ischemia in vivo, were studied. Changes in the adenine nucleotide pool, cell volume regulation, myocardial Ca and ultrastructure were studied at the end of 15 min of ischemia and after 0.5, 0.3 and 20 min of reflow. Before reperfusion, ATP and the adenylate pool decreased by 63% and 44% of control, respectively, and the adenylate charge was reduced to 0.65. After 3 min of reperfusion, the adenylate charge was restored to control by the rephosphorylation of adenosine mono- and diphosphate, but ATP was still reduced by 45%. Mild tissue edema was detected after 0.5 min of reflow and persisted throughout 20 min of reperfusion. Theincreased tissue H2O was accompanied by a slight increase in Na and a marked increase in tissue K. Although massive Ca accumulation develops when irreversibly injured tissue is reperfused, no Ca overload was detected during early reperfusion of reversibly injured myocytes. Reperfusion for 3 min exaggerated the mitochondrial swelling induced by 15 min of ischemia but after 20 min of reperfusion, myocardial ultrastructure was essentially normal except for rare swollen or disrupted, mitochondria. Thus, the cellular abnormalities associated with brief periods of ischemia persist for variable periods of time after reperfusion of reversibly injured myocytes. Although adenine nucleotide repletion occurs very slowly, the adenylate charge was restored after 3 min, indicating rapid resumption of mitochondrial ATP production. Ca overload was not detected, but myocardial edema and increased K persisted throughout the 20 min of reperfusion. The ultrastructural consequences of ischemia were nearly reversed after 20 min of reperfusion.