期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 281, 期 3, 页码 H1015-H1025出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2001.281.3.H1015
关键词
shear stress; pressure; conducted response; oxygen transport; mathematical modeling
资金
- NHLBI NIH HHS [HL-34555] Funding Source: Medline
Terminal vascular beds continually adapt to changing demands. A theoretical model is used to simulate structural diameter changes in response to hemodynamic and metabolic stimuli in microvascular networks. Increased wall shear stress and decreased intravascular pressure are assumed to stimulate diameter increase. Int avascular partial pressure of oxygen (PO2) is estimated for each segment. Decreasing PO2 is assumed to generate a metabolic stimulus for diameter increase, which acts locally, upstream via conduction along vessel walls, and downstream via metabolite convection. By adjusting the sensitivities to these stimuli, good agreement is achieved between predicted network characteristics and experimental data from microvascular networks in rat mesentery. Reduced pressure sensitivity leads to increased capillary pressure with reduced viscous energy dissipation and little change in tissue oxygenation. Dissipation decreases strongly with decreased metabolic response. Below a threshold level of metabolic response flow shifts to shorter pathways through the network, and oxygen supply efficiency decreases sharply. In summary, the distribution of vessel diameters generated by the simulated adaptive process allows the network to meet the functional demands of tissue while avoiding excessive viscous energy dissipation.
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