Orchard C H, Allen D G, Morris P G
Adv Myocardiol. 1985;6:417-27.
When oxidative metabolism is inhibited in heart muscle, developed tension often increases slightly before decreasing below control. We have examined the possible mechanisms underlying these changes in developed tension in two series of experiments. In the first series of experiments, the photoprotein aequorin was used to monitor intracellular free [Ca2+] [( Ca2+]i) in papillary muscles during inhibition of oxidative phosphorylation, using either cyanide or hypoxia. The observed changes of developed tension were independent of changes in [Ca2+]i. It was therefore possible that these changes of tension were due to changes of intracellular pH (pHi). We tested this idea in a second series of experiments, using 31P nuclear magnetic resonance to monitor pHi, [ATP], and phosphocreatine concentration [( PCr]) in Langendorff-perfused ferret hearts. During the application of cyanide, pHi increased transiently before decreasing to below control. [PCr] decreased throughout this period, but [ATP] did not change. It is concluded that the observed changes of pHi could account for most of the observed changes of developed tension. It is suggested that the initial increase of pHi is due to PCr breakdown and the subsequent decrease of pHi to accelerated anaerobic glycolysis.
当心肌中的氧化代谢受到抑制时，心肌产生的张力通常会在降至对照值以下之前先略有增加。我们在两个系列的实验中研究了这些张力变化背后的可能机制。在第一个系列实验中，利用光蛋白水母发光蛋白在使用氰化物或缺氧抑制氧化磷酸化过程中监测乳头肌细胞内游离钙离子浓度（[Ca2+]i）。观察到的张力变化与[Ca2+]i的变化无关。因此，这些张力变化可能是由于细胞内pH值（pHi）的变化所致。我们在第二个系列实验中验证了这一想法，使用31P核磁共振来监测Langendorff灌注雪貂心脏中的pHi、[ATP]和磷酸肌酸浓度（[PCr]）。在应用氰化物期间，pHi先短暂升高，然后降至对照值以下。在此期间，[PCr]持续下降，但[ATP]没有变化。结论是，观察到的pHi变化可以解释大部分观察到的张力变化。有人提出，pHi的最初升高是由于磷酸肌酸分解，随后pHi的下降是由于无氧糖酵解加速。
