Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses

Theoretical model of blood flow autoregulation: roles of myogenic, shear-dependent, and metabolic responses
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DOI:
10.1152/ajpheart.00262.2008
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发表时间:
2008-10-01
影响因子:
4.8
通讯作者:
Secomb, Timothy W.
Secomb, Timothy W.
中科院分区:
医学2区
文献类型:
--
作者:
Carlson, Brian E.;Arciero, Julia C.;Secomb, Timothy W.

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血流的自动调节,即在动脉压力变化的情况下维持几乎恒定的血流,是许多组织类型的特征。本文使用理论模型分析了压力依赖性、剪切应力依赖性和代谢血管活性反应的自调节作用。七个节段串联在一起,代表血管的种类:动脉、大微动脉、小微动脉、毛细血管、小静脉、大静脉和静脉。大动脉和小动脉积极响应局部压力和壁面剪切应力的变化,以及通过传导响应传达的下游代谢状态。所有其他段被认为是固定电阻。小动脉段的肌源性、剪切依赖性和代谢反应由基于分离血管实验数据的理论模型表示。为了评估自动调节,将动脉压为130 mmHg时的预测流量与80 mmHg时的预测流量进行比较。如果血管平滑肌的激活度保持在0.5,血流量会增加5倍。当包括张力的肌源性变化时,在相同的压力范围内,流量增加了1.66倍,表明自动调节较弱。包括肌源性和剪切依赖性反应导致流量增加2.43倍。进一步增加代谢反应产生强的自调节,流量增加1.18倍,结果与实验观察一致。模型结果表明,肌生成和代谢调节的联合作用克服了剪切反应的血管扩张作用,导致血流的自我调节。
The autoregulation of blood flow, the maintenance of almost constant blood flow in the face of variations in arterial pressure, is characteristic of many tissue types. Here, contributions to the autoregulation of pressure-dependent, shear stress-dependent, and metabolic vasoactive responses are analyzed using a theoretical model. Seven segments, connected in series, represent classes of vessels: arteries, large arterioles, small arterioles, capillaries, small venules, large venules, and veins. The large and small arterioles respond actively to local changes in pressure and wall shear stress and to the downstream metabolic state communicated via conducted responses. All other segments are considered fixed resistances. The myogenic, shear-dependent, and metabolic responses of the arteriolar segments are represented by a theoretical model based on experimental data from isolated vessels. To assess autoregulation, the predicted flow at an arterial pressure of 130 mmHg is compared with that at 80 mmHg. If the degree of vascular smooth muscle activation is held constant at 0.5, there is a fivefold increase in blood flow. When myogenic variation of tone is included, flow increases by a factor of 1.66 over the same pressure range, indicating weak autoregulation. The inclusion of both myogenic and shear-dependent responses results in an increase in flow by a factor of 2.43. A further addition of the metabolic response produces strong autoregulation with flow increasing by a factor of 1.18 and gives results consistent with experimental observation. The model results indicate that the combined effects of myogenic and metabolic regulation overcome the vasodilatory effect of the shear response and lead to the autoregulation of blood flow.