Mechanisms of myocardium-coronary vessel interaction
Mechanisms of myocardium-coronary vessel interaction
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DOI：
10.1152/ajpheart.00925.2009
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发表时间：
2010-03-01
影响因子：
4.8
通讯作者：
Lanir, Yoram
中科院分区：
文献类型：
--
作者：
Algranati, Dotan;Kassab, Ghassan S.;Lanir, Yoram
Algranati D，卡萨布GS，Lanir Y.心肌-冠状血管相互作用的机制。美国生理学杂志心脏循环生理学298：H861-H873，2010年。首次发表于2009年12月4日; doi：10.1152/ajpheart.00925.2009。收缩心肌对冠状动脉血管施加血管外力（心肌内压，IMP）及其影响冠状动脉血流的机制仍不完全清楚。已经提出了几种心肌-血管相互作用（MVI）机制，但没有一种可以解释所有主要的血流特征。在本研究中，我们假设只有MVI机制的特定组合可以解释所有观察到的冠状动脉血流特征。基于物理学原理（质量守恒和力平衡）分析了基于真实数据的血管网络中的三种基本相互作用机制（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。通过应力分析耦合血管壁和心肌的力学特性，以模拟血管对内部血压和外部（心肌）机械载荷的响应。在每种MVI机制下确定跨壁动态血管压、直径和流速的预测值，并与报告数据进行比较。结果表明，这三种基本机制都不能单独解释测量数据。只有腔诱导的细胞外压和缩短诱导的肌内压的综合作用才与大多数测量结果具有良好的一致性。这些发现对于阐明IMP的物理基础和理解冠状动脉相位流以及冠状动脉和微循环疾病具有重要意义。
Algranati D, Kassab GS, Lanir Y. Mechanisms of myocardium-coronary vessel interaction. Am J Physiol Heart Circ Physiol 298: H861-H873, 2010. First published December 4, 2009; doi:10.1152/ajpheart.00925.2009.-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.