Lethal myocardial ischemic injury.
Lethal myocardial ischemic injury.
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发表时间：
1981-02
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通讯作者：
R. Jennings;K. Reimer
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作者：
R. Jennings;K. Reimer
本文综述了严重缺血心肌细胞从可逆性损伤阶段到致死性或不可逆性损伤阶段的生物学变化，特别强调了缺血对高能磷酸盐的产生和利用、腺嘌呤核苷酸库的破坏以及肌膜质膜损伤迹象的出现的影响。证据表明，在体内严重缺血中发生的事件基本上是相同的，在体外总缺血中发现的，除了缺血的生物学变化发展更慢，在体外总缺血比在体内严重缺血。损伤的较慢的时间过程，以及由体外完全缺血提供的损伤的均匀性，可以允许更精确地识别缺血性损伤中潜在的致死性细胞事件。在体内和体外缺血中，通过测量乳酸积累，估计了由无氧糖酵解产生的高能磷酸盐（HEP），并从预先形成的HEP储存的消耗估计了总HEP利用率。结果表明，缺血犬左心室所利用的HEP的80%至90%是由无氧糖酵解产生的。不可逆性的发生与组织的HEP和腺嘌呤核苷酸库的显著消耗以及通过糖酵解的能量产生的停止有关。无氧糖酵解的停止可能是由于濒死肌细胞的肌浆三磷酸腺苷（ATP）浓度低所致。除了上述变化外，不可逆损伤的组织还表现出肌膜质膜破坏的超微结构和功能证据。严重的HEP耗竭和膜损伤之间可能的关系，因果关系和其他方面进行了讨论。HEP耗竭（ATP <对照的3-8%）和膜损伤两者被认为是存在不可逆心肌缺血性损伤的客观迹象。然而，在目前，没有证据表明，这些变化是因果关系，无论是彼此或严重的体内缺血细胞死亡。
The biologic changes occurring in severely ischemic myocytes in vivo as the affected cells pass through the phase of reversible to the phase of lethal or irreversible injury are reviewed with special emphasis on the effect of ischemia on the production and utilization of highenergy phosphate, the destruction of the adenine nucleotide pool, and the appearance of signs of damage to the plasma membrane of the sarcolemma. Evidence is presented that indicates that the events occurring in severe ischemia in vivo are essentially identical to those found in total ischemia in vitro except that the biologic changes of ischemia develop more slowly in total ischemia in vitro than in severe ischemia in vivo. The slower time course of injury, together with the uniformity of injury provided by total ischemia in vitro, may allow for more precise identification of potential lethal cellular events in ischemic injury. The production of highenergy phosphates (HEP) from anaerobic glycolysis have been estimated in both in vivo and in vitro ischemia by the measurement of lactate accumulation, and total HEP utilization has been estimated from the depletion of stores of preformed HEP. The results show that between 80% and 90% of the HEP utilized by ischemic dog left ventricle is produced by anaerobic glycolysis. The onset of irreversibility is associated with marked depletion of the HEP and adenine nucleotide pools of the tissue and the cessation of energy production via glycolysis. The cessation of anaerobic glycolysis may be caused by the low sarcoplasmic, adenosine triphosphate (ATP) concentration of the dying myocyte. In addition to the foregoing changes, irreversibly injured tissue exhibits both ultrastructural and functional evidence of disruption of the plasmalemma of the sarcolemma. The possible relationships, causal and otherwise, between severe HEP depletion and membrane damage are discussed. Both HEP depletion (ATP < 3-8% of control) and membrane damage are considered to be objective signs of the presence of irreversible myocardial ischemic injury. However, at the present time, there is no proof that these changes are causally related either to each other or to cell death in severe in vivo ischemia.