MECHANICS OF ACTIVE CONTRACTION IN CARDIAC-MUSCLE .2. CYLINDRICAL MODELS OF THE SYSTOLIC LEFT-VENTRICLE
MECHANICS OF ACTIVE CONTRACTION IN CARDIAC-MUSCLE .2. CYLINDRICAL MODELS OF THE SYSTOLIC LEFT-VENTRICLE
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DOI：
10.1115/1.2895474
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发表时间：
1993-02-01
影响因子：
1.7
通讯作者：
MCCULLOCH, AD
中科院分区：
文献类型：
--
作者：
GUCCIONE, JM;WALDMAN, LK;MCCULLOCH, AD
采用收缩心肌模型，研究了不同的主动张力发展假设对完整左心室收缩期赤道区应力应变分布的影响。将三个心肌收缩模型合并到先前开发的被动左心室力学的圆柱形模型中[Guccione等人，ASME Journal of Biomechanical Engineering，第113卷，第113页]。42-55（1991）]。通过心脏收缩的一般“失活"模型预测的肌节长度和纤维应力[Guccione和McCulloch，ASME Journal of Biomechanical Engineering，第115卷，第115页]。72-81（1993）]与使用两种较不复杂的活性纤维应力模型计算的结果进行比较：在随时间变化的“弹性”模型中，等长张力发展由峰值细胞内钙浓度、收缩开始后的时间和肌节长度的函数计算;通过使用从失活模型导出的力-速度关系来缩放该等长张力，来制定“Hill "模型。对于相同的钙离子浓度，失活模型中的肌节缩短约0。收缩末期整个壁的厚度比其他模型小1 μ m。因此，完整心室中的肌纤维经受快速长度变化，这在正常心动周期的射血阶段期间引起失活。失活模型预测相当均匀的跨壁分布的纤维应力和跨纤维应力分布，几乎相同的径向分量。这三个分量与主应力不可区分。失活模型预测的收缩末期心室壁应变分布与犬左心室前游离壁的实验测量结果密切相关。
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 mum 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.