Haworth R A, Hunter D R, Berkoff H A
Circ Res. 1981 Nov;49(5):1119-28. doi: 10.1161/01.res.49.5.1119.
Isolated intact quiescent myocytes from the adult rat were used as a model system for investigating the determinants of contracture induced by metabolic deprivation. The model simulated the pattern of contracture and ATP decline seen in the intact heart during ischemia. Three new insights into the contracture process were gained: (1) in the quiescent cell system, the rate of onset of contracture was independent of external Ca2+, supporting the view that the Ca2+ dependence of the rate of onset in the whole heart is related to beat-dependent substrate utilization; (2) the second phase of ATP decline was paralleled by a decline in the percentage of cells which had not undergone contracture, suggesting that-in any cell-contracture is immediately preceded by a total loss of ATP; and (3) oligomycin delayed the onset of contracture by 55 +/- 12%, suggesting that mitochondrial ATPase activity is a significant drain on energy resources in the quiescent ischemic heart.
成年大鼠分离出的完整静止心肌细胞被用作研究代谢剥夺诱导挛缩的决定因素的模型系统。该模型模拟了缺血期间完整心脏中出现的挛缩和ATP下降模式。获得了关于挛缩过程的三个新见解：（1）在静止细胞系统中，挛缩开始的速率与细胞外Ca2+无关，支持了全心中挛缩开始速率对Ca2+的依赖性与搏动依赖性底物利用有关的观点；（2）ATP下降的第二阶段与未发生挛缩的细胞百分比下降平行，表明在任何细胞中，挛缩之前紧接着是ATP的完全丧失；（3）寡霉素将挛缩开始延迟了55±12%，表明线粒体ATP酶活性是静止缺血心脏能量资源的重要消耗因素。
