在肥厚性重塑和心力衰竭期间，心脏中的肌酸和磷酸池维持在能量最佳水平。
Creatine and phosphate pools are maintained at energetically optimal levels in the heart during hypertrophic remodeling and heart failure.
作者信息
Beard Daniel A, Wu Fan
机构信息
Department of Physiology, Medical College of Wisconsin, Milwaukee, WI 53226, USA.
出版信息
Annu Int Conf IEEE Eng Med Biol Soc. 2009;2009:4487-90. doi: 10.1109/IEMBS.2009.5333680.
The ability of mitochondria to oxidatively synthesize ATP from ADP and inorganic phosphate is compromised in the failing heart. Specifically, the magnitude of the free energy at which ATP is synthesized in heart failure is diminished compared to control. However the causal mechanisms involved are not clearly understood. Here we used computer simulation to analyze the impact of reduction in three cytoplasmic metabolic pools that is observed with hypertrophic remodeling and heart failure. Our simulations, which are validated based on in vivo data on phosphate metabolites in both the healthy and diseased heart, predict that, given a prescribed reduction in the total adenine nucleotide pool, the pools of total creatine and total exchangeable phosphate are maintained at levels that maintain the ATP hydrolysis potential of the heart at near the normal physiological value.
在衰竭心脏中，线粒体从二磷酸腺苷（ADP）和无机磷酸盐氧化合成三磷酸腺苷（ATP）的能力受到损害。具体而言，与对照组相比，心力衰竭时合成ATP的自由能幅度降低。然而，其中涉及的因果机制尚不清楚。在此，我们使用计算机模拟来分析在肥厚性重塑和心力衰竭中观察到的三个细胞质代谢池减少的影响。我们的模拟基于健康和患病心脏中磷酸盐代谢物的体内数据进行了验证，预测在总腺嘌呤核苷酸池规定减少的情况下，总肌酸池和总可交换磷酸盐池维持在一定水平，使心脏的ATP水解电位保持在接近正常生理值。
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