Jennings R B, Hawkins H K, Lowe J E, Hill M L, Klotman S, Reimer K A
Am J Pathol. 1978 Jul;92(1):187-214.
The relationship between progressive depletion of high energy phosphate and the onset of lethal cell injury in ischemic myocardium following coronary occlusion has been evaluated. Myocardial ischemia was induced by proximal occlusion of the circumflex coronary artery for 15, 30, 40, or 60 minutes. Cell injury in the severely ischemic posterior papillary muscle (PP) was evaluated by electron microscopy and by measuring the capacity of slices of the injured PP to maintain electrolytes, resynthesize high energy phosphate, and exclude inulin during in vitro incubation. ATP content in the ischemic myocardium decreased to 35%, 9%, 7%, and 5% of control values after 15, 30, 40, and 60 minutes of ischemia, respectively, and was associated with a corresponding depletion of total adenine nucleotides. The loss of 65% of the ATP after 15 minutes of ischemia (reversible injury) was associated with only minimal ultrastructural changes and no significant defects of electrolytes in incubated slices. However, the depletion of over 90% of the ATP after 40 minutes of ischemia (irreversible injury) was associated with significant fine structural changes and markedly altered cell volume regulation. The results suggest a close relationship between the marked depletion of high energy phsophates and the development of lethal injury in acutely ischemic myocardium.
已经评估了高能磷酸盐的逐渐耗竭与冠状动脉闭塞后缺血心肌中致死性细胞损伤发作之间的关系。通过旋支冠状动脉近端闭塞15、30、40或60分钟诱导心肌缺血。通过电子显微镜以及通过测量受损后乳头肌（PP）切片在体外孵育期间维持电解质、重新合成高能磷酸盐和排除菊粉的能力来评估严重缺血的后乳头肌（PP）中的细胞损伤。缺血心肌中的ATP含量在缺血15、30、40和60分钟后分别降至对照值的35%、9%、7%和5%，并且与总腺嘌呤核苷酸的相应消耗相关。缺血15分钟后ATP损失65%（可逆性损伤）仅伴有最小的超微结构变化，并且孵育切片中的电解质没有明显缺陷。然而，缺血40分钟后ATP消耗超过90%（不可逆性损伤）与明显的精细结构变化和明显改变的细胞体积调节相关。结果表明高能磷酸盐的明显消耗与急性缺血心肌中致死性损伤的发展之间存在密切关系。
