Department of Mechanical and Aerospace Engineering, University of California-San Diego, La Jolla, California 92093-0412, USA.
Am J Physiol Heart Circ Physiol. 2012 Nov 1;303(9):H1096-106. doi: 10.1152/ajpheart.00438.2012. Epub 2012 Aug 24.
Here, we present an analytic model of arteriolar mechanics that accounts for key autoregulation mechanisms, including the myogenic response and the vasodilatory effects of nitric oxide (NO) in the vasculature. It couples the fluid mechanics of blood flow in arterioles with solid mechanics of the vessel wall and includes the effects of wall shear stress- and stretch-induced endothelial NO production. The model can be used to describe the regulation of blood flow and NO transport under small changes in hematocrit and to analyze the regulatory response of arterioles to small changes in hematocrit. Our analysis revealed that the experimentally observed paradoxical increase in cardiac output with small increases in hematocrit results from the combination of increased NO production and the effects of a strong myogenic response modulated by elevated levels of WSS. Our findings support the hypothesis that vascular resistance varies inversely with blood viscosity for small changes in hematocrit in a healthy circulation that responds to shear stress stimuli. They also suggest beneficial effects independent of changes in O(2) carrying capacity associated with the postsurgical transfusion of one or two units of blood.
在这里，我们提出了一个动静脉力学分析模型，该模型考虑了关键的自动调节机制，包括血管中的肌源性反应和一氧化氮（NO）的血管舒张作用。它将动静脉中的血流流体力学与血管壁的固体力学结合起来，并包括壁切应力和拉伸诱导的内皮细胞 NO 产生的影响。该模型可用于描述血液黏度小变化时的血流量和 NO 运输的调节，并分析动静脉对血液黏度小变化的调节反应。我们的分析表明，实验观察到的血液黏度小增加时心输出量的反常增加是由于 NO 产生增加以及由升高的壁切应力水平调节的强烈肌源性反应的影响共同作用的结果。我们的研究结果支持这样一种假说，即在健康循环中，血液黏度小变化时，血管阻力与血液黏度成反比，循环会对切应力刺激做出反应。它们还表明，与手术后输注一个或两个单位的血液相关的携氧能力变化无关的有益作用。
