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A calcium-driven mechanochemical model for prediction of force generation in smooth muscle

机译:钙驱动的机械化学模型,用于预测平滑肌中的力生成

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A new model for the mechanochemical response of smooth muscle is presented. The focus is on the res- ponse of the actin-myosin complex and on the related generation of force (or stress). The chemical (kinetic) model describes the cross-bridge interactions with the thin filament in which the calcium-dependent myosin phosphorylation is the only regulatory mechanism. The new mechanical model is based on Hill's three-component model and it includes one internal state variable that describes the contraction/relaxation of the contractile units. It is characterized by a strain-energy function and an evolution law incorporating only a few material parameters with clear physical meaning. The proposed model satisfies the second law of thermodynamics. The results of the combined coupled model are broadly consistent with isometric and isotonic experiments on smooth muscle tissue. The simulations suggest that the matrix in which the actin-myosin complex is embedded does have a viscous property. It is straightforward for implementation into a finite element program in order to solve more complex boundary-value problems such as the control of short-term changes in lumen diameter of arteries due to mechanochemical signals.
机译:提出了一种新的平滑肌机械化学反应模型。重点是肌动蛋白-肌球蛋白复合物的反应以及相关的力(或压力)产生。化学(动力学)模型描述了与细丝的跨桥相互作用,其中钙依赖性肌球蛋白磷酸化是唯一的调节机制。新的机械模型基于Hill的三分量模型,并且包含一个内部状态变量,该变量描述了收缩单位的收缩/松弛。它的特征在于应变能函数和仅包含少数具有明确物理意义的材料参数的演化规律。所提出的模型满足热力学第二定律。组合耦合模型的结果与平滑肌组织的等距和等渗实验大致一致。模拟表明肌动蛋白-肌球蛋白复合物嵌入其中的基质确实具有粘性。为了解决更复杂的边界值问题,例如控制由于机械化学信号引起的动脉管腔直径的短期变化,将其实施到有限元程序中非常简单。

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