Nguyen Phuc H, Tuzun Egemen, Quick Christopher M
Michael E. DeBakey Institute, Texas A&M University, College Station, Texas; and.
Texas A&M Institute for Preclinical Studies, College Station, Texas.
Am J Physiol Regul Integr Comp Physiol. 2016 Sep 1;311(3):R522-31. doi: 10.1152/ajpregu.00402.2015. Epub 2016 Jun 15.
Aortic pulse pressure arises from the interaction of the heart, the systemic arterial system, and peripheral microcirculations. The complex interaction between hemodynamics and arterial remodeling precludes the ability to experimentally ascribe changes in aortic pulse pressure to particular adaptive responses. Therefore, the purpose of the present work was to use a human systemic arterial system model to test the hypothesis that pulse pressure homeostasis can emerge from physiological adaptation of systemic arteries to local mechanical stresses. First, we assumed a systemic arterial system that had a realistic topology consisting of 121 arterial segments. Then the relationships of pulsatile blood pressures and flows in arterial segments were characterized by standard pulse transmission equations. Finally, each arterial segment was assumed to remodel to local stresses following three simple rules: 1) increases in endothelial shear stress increases radius, 2) increases in wall circumferential stress increases wall thickness, and 3) increases in wall circumferential stress decreases wall stiffness. Simulation of adaptation by iteratively calculating pulsatile hemodynamics, mechanical stresses, and vascular remodeling led to a general behavior in response to mechanical perturbations: initial increases in pulse pressure led to increased arterial compliances, and decreases in pulse pressure led to decreased compliances. Consequently, vascular adaptation returned pulse pressures back toward baseline conditions. This behavior manifested when modeling physiological adaptive responses to changes in cardiac output, changes in peripheral resistances, and changes in local arterial radii. The present work, thus, revealed that pulse pressure homeostasis emerges from physiological adaptation of systemic arteries to local mechanical stresses.
主动脉脉压源于心脏、体循环动脉系统和外周微循环之间的相互作用。血液动力学与动脉重塑之间复杂的相互作用使得无法通过实验将主动脉脉压的变化归因于特定的适应性反应。因此，本研究的目的是使用人体体循环动脉系统模型来检验以下假设：脉压稳态可通过体循环动脉对局部机械应力的生理适应而出现。首先，我们假定一个具有现实拓扑结构的体循环动脉系统，该系统由121个动脉段组成。然后，通过标准的脉搏传播方程来描述动脉段中脉动血压与血流之间的关系。最后，假定每个动脉段根据三条简单规则重塑以适应局部应力：1）内皮剪切应力增加会使半径增大；2）壁周向应力增加会使壁厚增加；3）壁周向应力增加会使壁硬度降低。通过迭代计算脉动血液动力学、机械应力和血管重塑来模拟适应过程，结果显示出对机械扰动的一般反应：脉压最初增加会导致动脉顺应性增加，脉压降低会导致顺应性降低。因此，血管适应使脉压恢复到基线状态。在对心输出量变化、外周阻力变化和局部动脉半径变化进行生理适应性反应建模时，这种行为均有体现。因此，本研究揭示了脉压稳态是通过体循环动脉对局部机械应力的生理适应而出现的。
