Chinet A, Ventura-Clapier R, Vassort G
University Department of Physiology, C.M.U., Geneva, Switzerland.
J Mol Cell Cardiol. 1993 Feb;25(2):145-57. doi: 10.1006/jmcc.1993.1018.
Energy dissipation and the bearing of tension during ionic contracture in myocardium may not result from one and the same process. To test this, comparative indirect and direct microcalorimetry determinations were made in non-perfused tissue-cell preparations under optimal oxygenation conditions (right papillary muscles, high-pO2 superfusion, 30 degrees C) before, during and after exposure to low-Na, high-K solutions. Over a 15-min contracture plus 45-min recovery cycle, both heat production rate (E), and the indirectly determined heat production rate (EO2) which is oxygen uptake multiplied by the overall energetic equivalent of O2 for nutrient oxidations, were constantly larger than basal rates. The two 60-min time integrals of this increase in metabolic rate were equal [30.3 +/- 3.7 and 31.0 +/- 3.9 (SE) J/g muscle wet weight (n = 9) for E and EO2 respectively]. During contracture however, E exceeded EO2 by 24% (4.7 +/- 1.7 J/g), and during the recovery period EO2 exceeded E by 21% (5.4 +/- 2.6 J/g). Whereas oxidative recovery of the energy lost by the preparation during 15-min contractures was complete, after longer contractures recovery did not occur or was incomplete. In keeping with the now prevalent idea that ion--namely Ca--transport activities are maintained foremost among cellular ATP-dependent processes and consume significant amounts of energy, the present finding that in a 15-min ionic contracture myocardium incurs not only some, but the maximum oxygen debt still compatible with complete oxidative recovery suggests that contracture tension is maintained at low energy cost, essentially by slow-cycling or "rigor" bridges as in hypoxic contractures, whereas heat is mainly related to intracellular calcium homeostasis.
心肌离子性挛缩期间的能量耗散和张力承受可能并非源于同一过程。为验证这一点，在最佳氧合条件下（右乳头肌、高pO₂灌注、30℃），对未灌注的组织 - 细胞制剂在暴露于低钠、高钾溶液之前、期间和之后进行了比较间接和直接微量量热法测定。在15分钟挛缩加45分钟恢复周期内，产热率（E）以及间接测定的产热率（EO₂，即氧气摄取量乘以营养物氧化中O₂的总能量当量）始终高于基础速率。代谢率增加的这两个60分钟时间积分相等[E和EO₂分别为30.3±3.7和31.0±3.9（SE）J/g肌肉湿重（n = 9）]。然而，在挛缩期间，E比EO₂高24%（4.7±1.7 J/g），而在恢复期间，EO₂比E高21%（5.4±2.6 J/g）。虽然制剂在15分钟挛缩期间损失的能量的氧化恢复是完全的，但较长时间挛缩后恢复未发生或不完全。与目前普遍的观点一致，即离子（即Ca）转运活动在细胞ATP依赖过程中最为重要且消耗大量能量，目前的发现表明，在15分钟的离子性挛缩中，心肌不仅产生了一些，而且产生了与完全氧化恢复仍相容的最大氧债，这表明挛缩张力基本上通过慢循环或“强直”桥维持在低能量成本，就像在缺氧性挛缩中一样，而热量主要与细胞内钙稳态有关。
