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基于主动横桥模型估算的心肌横桥循环能量

Cross-bridge cycling energy of cardiac muscle estimated from an active cross-bridge model.

作者信息

Takeda K, Yagi S

机构信息

Department of Medicine, Dokkyo University School of Medicine, Tochigi, Japan.

出版信息

Jpn Heart J. 1991 Jan;32(1):69-89. doi: 10.1536/ihj.32.69.

Abstract

A mathematical formula was derived from an active cross-bridge model to express the changes in the active myocardial force which occurred during systole. Using the formula and the assumption that the energy expenditure for cross-bridge cycling (Um) was a linear function of the force-time integral (FTI), we developed formulae describing the left ventricular Um versus FTI relation, the Um versus force relation, and the Um versus pressure-volume area (PVA) relation. There were strong disagreements between the model predictions and the experimental findings relating oxygen consumption of the heart versus the PVA relation. These differences may have resulted from the oversimplification of important mechanical and/or biochemical properties of the myocardium in the model. However, the model appeared to accurately reproduce the Fenn effect (effect of contraction modes on energy liberation) for the myocardium as well as the effect of catecholamine infusion, hypothermia, and hypothyroidism on the changes in the binding rate of Ca2+ with the regulatory proteins, the myosin ATPase activity, the peak force developed, and the myocardial energy expenditure. We present this work as an intermediate step towards a complete theoretical linkage between the molecular biology, dynamics, and energetics of the human heart.

摘要

从一个活性横桥模型推导出一个数学公式,以表达在收缩期发生的活性心肌力的变化。利用该公式,并假设横桥循环的能量消耗(Um)是力-时间积分(FTI)的线性函数,我们推导了描述左心室Um与FTI关系、Um与力关系以及Um与压力-容积面积(PVA)关系的公式。模型预测结果与关于心脏耗氧量与PVA关系的实验结果之间存在很大分歧。这些差异可能是由于模型中对心肌重要力学和/或生化特性的过度简化所致。然而,该模型似乎能准确再现心肌的芬恩效应(收缩模式对能量释放的影响)以及儿茶酚胺输注、低温和甲状腺功能减退对Ca2+与调节蛋白结合率变化、肌球蛋白ATP酶活性、产生的峰值力和心肌能量消耗的影响。我们将这项工作作为朝着人类心脏分子生物学、动力学和能量学之间完整理论联系迈出的中间步骤呈现出来。

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