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A distribution-moment model of deactivation in cardiac muscle.

机译:心肌失活的分布矩模型。

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The Distribution Moment (DM) model has simulated experimental data on skeletal muscle, but it has not been used previously to study the mechanics of active contraction in cardiac muscle. In contrast to previous models of striated muscle contraction, all parameters have physical meaning and assumptions concerning biophysical events within the cell are consistent with available data. In order to simulate cardiac muscle deactivation using the DM model it was necessary to make the cross-bridge detachment rates large for large displacements from the neutral equilibrium position of a cross-bridge. To examine the effect of cooperativity on cardiac muscle contraction, we used the DM model's tight coupling scheme with binding of one or two calcium sites regulating contraction. As observed experimentally, our model predicted a reduction of isometric tension development following rapid shortening lengthening transients when contraction is regulated by either one or two calcium binding sites. The predicted deactivating effect increased if the transient was applied late in the twitch when contraction is regulated by two calcium binding sites, but not when it is regulated by one site. This is the first study in which deactivation has been simulated without making any provisions for length-dependent calcium trononin dissociation.
机译:分布矩(DM)模型已经模拟了骨骼肌的实验数据,但是之前尚未用于研究心肌主动收缩的机制。与以前的横纹肌收缩模型相反,所有参数都具有物理意义,并且有关细胞内生物物理事件的假设与可用数据一致。为了使用DM模型模拟心肌失活,有必要使跨桥的分离速度大,以防止从跨桥的中性平衡位置发生较大位移。为了检查协同性对心肌收缩的影响,我们使用了DM模型的紧密耦合方案,结合了一个或两个调节收缩的钙位。正如实验观察到的那样,当收缩受一个或两个钙结合位点调节时,我们的模型预测等距张力的发展会随着快速缩短的延长瞬变而减少。如果在两个钙结合位点调节收缩时在抽搐后期应用瞬态,则预期的失活作用会增强,但在一个位点调节收缩时则不会。这是第一项模拟失活的研究,没有为长度依赖性钙肌钙蛋白解离做任何准备。

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