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心肌-冠状动脉相互作用的机制。

Mechanisms of myocardium-coronary vessel interaction.

机构信息

Faculty of Biomedical Engineering, Technion, Haifa, Israel.

出版信息

Am J Physiol Heart Circ Physiol. 2010 Mar;298(3):H861-73. doi: 10.1152/ajpheart.00925.2009. Epub 2009 Dec 4.

Abstract

The mechanisms by which the contracting myocardium exerts extravascular forces (intramyocardial pressure, IMP) on coronary blood vessels and by which it affects the coronary flow remain incompletely understood. Several myocardium-vessel interaction (MVI) mechanisms have been proposed, but none can account for all the major flow features. In the present study, we hypothesized that only a specific combination of MVI mechanisms can account for all observed coronary flow features. Three basic interaction mechanisms (time-varying elasticity, myocardial shortening-induced intracellular pressure, and ventricular cavity-induced extracellular pressure) and their combinations were analyzed based on physical principles (conservation of mass and force equilibrium) in a realistic data-based vascular network. Mechanical properties of both vessel wall and myocardium were coupled through stress analysis to simulate the response of vessels to internal blood pressure and external (myocardial) mechanical loading. Predictions of transmural dynamic vascular pressure, diameter, and flow velocity were determined under each MVI mechanism and compared with reported data. The results show that none of the three basic mechanisms alone can account for the measured data. Only the combined effect of the cavity-induced extracellular pressure and the shortening-induced intramyocyte pressure provides good agreement with the majority of measurements. These findings have important implications for elucidating the physical basis of IMP and for understanding coronary phasic flow and coronary artery and microcirculatory disease.

摘要

心肌收缩时向冠状动脉施加血管外作用力(心肌内压,IMP)的机制以及影响冠状动脉血流的机制尚未完全阐明。已经提出了几种心肌-血管相互作用(MVI)机制,但没有一种机制可以解释所有主要的血流特征。在本研究中,我们假设只有特定的 MVI 机制组合才能解释所有观察到的冠状动脉血流特征。基于物理原理(质量守恒和力平衡),在基于真实数据的血管网络中分析了三种基本的相互作用机制(时变弹性、心肌缩短引起的细胞内压力和心室腔引起的细胞外压力)及其组合。通过应力分析将血管壁和心肌的力学特性耦合在一起,以模拟血管对内部血压和外部(心肌)机械加载的反应。在每种 MVI 机制下确定了跨壁动态血管压力、直径和流速的预测值,并与报道的数据进行了比较。结果表明,这三种基本机制单独作用都不能解释测量数据。只有腔室诱导的细胞外压力和缩短诱导的细胞内压力的联合作用与大多数测量结果吻合良好。这些发现对于阐明 IMP 的物理基础以及理解冠状动脉时相性血流和冠状动脉及微循环疾病具有重要意义。

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