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心肌主动收缩机制:第二部分——收缩期左心室的圆柱模型。

Mechanics of active contraction in cardiac muscle: Part II--Cylindrical models of the systolic left ventricle.

作者信息

Guccione J M, Waldman L K, McCulloch A D

机构信息

Department of Biomedical Engineering, Johns Hopkins University, School of Medicine, Baltimore, Maryland 21205.

出版信息

J Biomech Eng. 1993 Feb;115(1):82-90. doi: 10.1115/1.2895474.

Abstract

Models of contracting ventricular myocardium were used to study the effects of different assumptions concerning active tension development on the distributions of stress and strain in the equatorial region of the intact left ventricle during systole. Three models of cardiac muscle contraction were incorporated in a cylindrical model for passive left ventricular mechanics developed previously [Guccione et al. ASME Journal of Biomechanical Engineering, Vol. 113, pp. 42-55 (1991)]. Systolic sarcomere length and fiber stresses predicted by a general "deactivation" model of cardiac contraction [Guccione and McCulloch, ASME Journal of Biomechanical Engineering, Vol. 115, pp. 72-81 (1993)] were compared with those computed using two less complex models of active fiber stress: In a time-varying "elastance" model, isometric tension development was computed from a function of peak intracellular calcium concentration, time after contraction onset and sarcomere length; a "Hill" model was formulated by scaling this isometric tension using the force-velocity relation derived from the deactivation model. For the same calcium ion concentration, the sarcomeres in the deactivation model shortened approximately 0.1 microns less throughout the wall at end-systole than those in the other models. Thus, muscle fibers in the intact ventricle are subjected to rapid length changes that cause deactivation during the ejection phase of a normal cardiac cycle. The deactivation model predicted rather uniform transmural profiles of fiber stress and cross-fiber stress distributions that were almost identical to those of the radial component. These three components were indistinguishable from the principal stresses. Transmural strain distributions predicted at end-systole by the deactivation model agreed closely with experimental measurements from the anterior free wall of the canine left ventricle.

摘要

利用心室心肌收缩模型,研究了关于主动张力发展的不同假设对完整左心室收缩期赤道区域应力和应变分布的影响。将三种心肌收缩模型纳入先前开发的被动左心室力学圆柱模型中[Guccione等人,《美国机械工程师学会生物医学工程杂志》,第113卷,第42 - 55页(1991年)]。将心脏收缩的一般“失活”模型[Guccione和McCulloch,《美国机械工程师学会生物医学工程杂志》,第115卷,第72 - 81页(1993年)]预测的收缩期肌节长度和纤维应力与使用两种不太复杂的主动纤维应力模型计算的结果进行了比较:在时变“弹性”模型中,等长张力发展根据细胞内钙浓度峰值、收缩开始后的时间和肌节长度的函数进行计算;“希尔”模型通过使用从失活模型导出的力 - 速度关系对该等长张力进行缩放来构建。对于相同的钙离子浓度,在收缩末期,失活模型中的肌节在整个壁内比其他模型中的肌节缩短约0.1微米。因此,完整心室中的肌纤维在正常心动周期的射血期会经历导致失活的快速长度变化。失活模型预测的纤维应力和跨纤维应力分布的透壁轮廓相当均匀,几乎与径向分量的轮廓相同。这三个分量与主应力难以区分。失活模型在收缩末期预测的透壁应变分布与犬左心室前游离壁的实验测量结果密切吻合。

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