Theoretical model of metabolic blood flow regulation: roles of ATP release by red blood cells and conducted responses
Theoretical model of metabolic blood flow regulation: roles of ATP release by red blood cells and conducted responses
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DOI：
10.1152/ajpheart.00261.2008
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发表时间：
2008-10-01
影响因子：
4.8
通讯作者：
Secomb, Timothy W.
中科院分区：
文献类型：
--
作者：
Arciero, Julia C.;Carlson, Brian E.;Secomb, Timothy W.
一种提出的代谢流调节机制涉及红细胞ATP的饱和依赖性释放，其触发上游传导响应信号和小动脉血管舒张。为了分析这一机制，使用理论模型来模拟氧气和ATP水平沿着七个代表性的部分，包括两个血管活性小动脉段的流动路径的变化。传导响应信号通过沿血管通路沿着积分ATP浓度来定义，假设信号在上游方向上的指数衰减，长度常数类似于1 cm。小动脉张力取决于传导的代谢信号和局部壁剪切应力和壁张力。根据血管平滑肌力学计算小动脉直径。该模型预测，在小静脉和传播到小动脉的ATP释放刺激的传导反应可以解释增加灌注响应于增加的氧气需求是一致的实验结果在低到中等的耗氧率。肌源性和剪切依赖性反应被发现与这种代谢流调节机制相反。
A proposed mechanism for metabolic flow regulation involves the saturation-dependent release of ATP by red blood cells, which triggers an upstream conducted response signal and arteriolar vasodilation. To analyze this mechanism, a theoretical model is used to simulate the variation of oxygen and ATP levels along a flow pathway of seven representative segments, including two vasoactive arteriolar segments. The conducted response signal is defined by integrating the ATP concentration along the vascular pathway, assuming exponential decay of the signal in the upstream direction with a length constant of similar to 1 cm. Arteriolar tone depends on the conducted metabolic signal and on local wall shear stress and wall tension. Arteriolar diameters are calculated based on vascular smooth muscle mechanics. The model predicts that conducted responses stimulated by ATP release in venules and propagated to arterioles can account for increases in perfusion in response to increased oxygen demand that are consistent with experimental findings at low to moderate oxygen consumption rates. Myogenic and shear-dependent responses are found to act in opposition to this mechanism of metabolic flow regulation.