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Adaptation of cardiac structure by mechanical feedback in the environment of the cell: a model study.

机译:在细胞环境中通过机械反馈适应心脏结构:模型研究。

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摘要

In the cardiac left ventricle during systole mechanical load of the myocardial fibers is distributed uniformly. A mechanism is proposed by which control of mechanical load is distributed over many individual control units acting in the environment of the cell. The mechanics of the equatorial region of the left ventricle was modeled by a thick-walled cylinder composed of 6-1500 shells of myocardial fiber material. In each shell a separate control unit was simulated. The direction of the cells was varied so that systolic fiber shortening approached a given optimum of 15%. End-diastolic sarcomere length was maintained at 2.1 microns. Regional early-systolic stretch and global contractility stimulated growth of cellular mass. If systolic shortening was more than normal the passive extracellular matrix stretched. The design of the load-controlling mechanism was derived from biological experiments showing that cellular processes are sensitive to mechanical deformation. After simulating a few hundred adaptation cycles, the macroscopic anatomical arrangement of helical pathways of the myocardial fibers formed automatically. If pump load of the ventricle was changed, wall thickness and cavity volume adapted physiologically. We propose that the cardiac anatomy may be defined and maintained by a multitude of control units for mechanical load, each acting in the cellular environment. Interestingly, feedback through fiber stress is not a compelling condition for such control.
机译:在心脏收缩期间,心肌纤维的机械负荷在心脏左心室中均匀分布。提出了一种机制,通过该机制,机械负荷的控制分布在作用于电池环境中的许多单独的控制单元上。左心室赤道区域的力学模型是由一个厚壁圆柱体模拟的,该圆柱体由6-1500个心肌纤维材料制成。在每个外壳中,都模拟了一个单独的控制单元。细胞的方向是变化的,因此收缩纤维缩短达到了给定的15%的最佳值。舒张末期肌节长度保持在2.1微米。区域早期收缩舒张和全球收缩刺激细胞质量的增长。如果收缩期缩短程度超过正常水平,则被动细胞外基质会拉伸。负载控制机制的设计源自生物学实验,表明细胞过程对机械变形敏感。在模拟了数百个适应循环后,心肌纤维螺旋路径的宏观解剖学排列自动形成。如果心室的泵负荷改变,则壁厚和腔体积在生理上适应。我们建议可以通过多个控制单元来定义和维护心脏解剖结构,每个控制单元都作用于细胞环境中。有趣的是,通过纤维应力进行反馈并不是强制控制的条件。

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