A distribution-moment model of deactivation in cardiac muscle.
A distribution-moment model of deactivation in cardiac muscle.
复制标题
心肌失活的分布矩模型。
DOI：
10.1016/s0021-9290(98)00120-1
复制
发表时间：
1998
影响因子：
2.4
通讯作者：
Zahalak,GI
中科院分区：
文献类型：
--
作者：
Guccione,JM;Motabarzadeh,I;Zahalak,GI
分布矩（DM）模型模拟了骨骼肌的实验数据，但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比，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现有数据一致。为了使用DM模型模拟心肌失活，有必要使跨桥脱离速率从跨桥的中性平衡位置大位移。为了检验协同性对心肌收缩的影响，我们采用DM模型的紧密耦合方案，结合一个或两个钙位点调节收缩。根据实验观察，我们的模型预测，当收缩由一个或两个钙结合位点调节时，在快速缩短-延长瞬态后，等长张力发展会减少。当收缩受两个钙结合位点调控时，在抽搐后期施加瞬时电流，预测的失活效果会增加，而当收缩受一个位点调控时，预测的失活效果则不会增加。这是第一个模拟失活的研究，没有对长度依赖性钙-钙钠蛋白解离作出任何规定。
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.