Beyar R, Dong S J, Smith E R, Belenkie I, Tyberg J V
Department of Medicine and Medical Physiology, University of Calgary, Alberta, Canada.
Am J Physiol. 1993 Dec;265(6 Pt 2):H2044-56. doi: 10.1152/ajpheart.1993.265.6.H2044.
Diastolic ventricular interaction is associated with septal shift and deformation, the consequences of which have not been fully assessed. A model was therefore developed to describe the mechanisms involved in interaction between the ventricles under different loading conditions. We assumed a circular cardiac minor-axis geometry surrounded by a pericardial membrane with the left ventricle (LV) and septum described by three layers. To define the equilibrium condition, we required the net force-balance at the right ventricular (RV)-LV intersection points to equal zero. The model was tested with and without consideration of bending forces associated with a change of curvature of a thick-walled structure. Model results were compared with data from animal experiments subjected to aortic and pulmonary constriction. LV and RV end-diastolic pressures as well as pericardial pressure were measured. In six dogs, septal segment length was measured using sonomicrometry, and in seven dogs, endocardial curvature was measured using echocardiography. Model and experimental results show that 1) with severe RV loading, septal inversion occurs at a negative transseptal gradient, and 2) the end-diastolic septal segment length continues to shorten after septal inversion during pulmonary constriction. Model simulation suggests that bending moments account for the septal curvature at zero transseptal pressure. In addition, the model predicts the shift in the pressure-area relationship of each ventricle by a change in loading of the opposite ventricle and predicts that large transmural gradients in stress and strain are associated with septal inversion. Thus the model and the experimental data agree and describe the important factors that modulate diastolic septal mechanics during acute differential ventricular loading.
舒张期心室相互作用与室间隔移位和变形有关,但其后果尚未得到充分评估。因此,开发了一个模型来描述不同负荷条件下心室之间相互作用所涉及的机制。我们假设心脏短轴呈圆形,周围有心包膜,左心室(LV)和室间隔由三层组成。为了定义平衡条件,我们要求右心室(RV)-LV交点处的净力平衡等于零。该模型在考虑和不考虑与厚壁结构曲率变化相关的弯曲力的情况下进行了测试。将模型结果与主动脉和肺动脉缩窄动物实验的数据进行了比较。测量了LV和RV舒张末期压力以及心包压力。在6只狗中,使用超声心动图测量室间隔节段长度,在7只狗中,使用超声心动图测量心内膜曲率。模型和实验结果表明:1)在严重RV负荷下,室间隔反转发生在负跨间隔梯度时;2)在肺缩窄期间,室间隔反转后舒张末期室间隔节段长度继续缩短。模型模拟表明,弯矩是跨间隔压力为零时室间隔曲率的原因。此外,该模型通过对侧心室负荷的变化预测每个心室压力-面积关系的变化,并预测应力和应变中的大跨壁梯度与室间隔反转有关。因此,模型和实验数据一致,并描述了急性差异性心室负荷期间调节舒张期室间隔力学的重要因素。