Piper H M, Schwartz P, Spahr R, Hütter J F, Spieckermann P G
Pflugers Arch. 1984 May;401(1):71-6. doi: 10.1007/BF00581535.
Cultured adult cardiac myocytes were exposed to anoxia under substrate-free conditions and then reoxygenated. When comparing the oxygen deficient organ to the anoxic cell culture, we see that metabolic changes in the latter system proceed in a similar, yet prolonged manner, as in arrested hearts. Release of cytosolic enzymes starts with minor energetic disturbances and proceeds closely correlated to the actual ATP level. Below 2 mumol ATP/gww, an increasing number of cells becomes irreversibly damaged, above this level, 30 min reoxygenation leads to extensive recovery of the whole preparation. The results indicate that leakage of cytosolic enzymes during the early stage of anoxia is due to a gradual protein release from the individual cells and is related to reversible membrane alterations. Reoxygenation does not induce changes considered typical of the 'oxygen paradox'. Since mechanical cell-cell interactions are absent in this model, it is suggested that aggravation of tissue damage in heart tissue reoxygenated late is mainly caused by mechanical forces.
将成年心肌细胞在无底物条件下进行缺氧处理，然后再进行复氧。当将缺氧的器官与缺氧的细胞培养物进行比较时，我们发现后一种系统中的代谢变化与停搏心脏中的代谢变化相似，但持续时间更长。胞质酶的释放始于轻微的能量紊乱，并与实际的ATP水平密切相关。当ATP低于2微摩尔/克湿重时，越来越多的细胞会受到不可逆的损伤，高于此水平，30分钟的复氧可使整个制剂得到广泛恢复。结果表明，缺氧早期胞质酶的泄漏是由于单个细胞逐渐释放蛋白质，并且与可逆的膜改变有关。复氧不会诱导被认为是“氧悖论”典型的变化。由于该模型中不存在机械性细胞间相互作用，因此提示晚期复氧的心脏组织中组织损伤的加重主要是由机械力引起的。
