期刊
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
卷 279, 期 2, 页码 H657-H671出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajpheart.2000.279.2.H657
关键词
microcirculation; oxygen diffusion; endothelial cell; smooth muscle cell; arterioles; nitric oxide
资金
- NHLBI NIH HHS [HL-18292] Funding Source: Medline
The problem of diffusion of O-2 across the endothelial surface in precapillary vessels and its utilization in the vascular wall remains unresolved. To establish a relationship between precapillary release of O-2 and vascular wall consumption, we estimated the intravascular flux of O-2 on the basis of published in vivo measurements. To interpret the data, we utilized a diffusion model of the vascular wall and computed possible physiological ranges for O-2 consumption. We found that many flux values were not consistent with the diffusion model. We estimated the mitochondrial-based maximum O-2 consumption of the vascular wall (M-mt) and a possible contribution to O-2 consumption of nitric oxide production by endothelial cells (MNO). Many values of O-2 consumption predicted from the diffusion model exceeded M-mt + M-NO. In contrast, reported values of O-2 consumption for endothelial and smooth muscle cell suspensions and vascular strips in vitro do not exceed M-mt. We conjecture that most of the reported values of intravascular O-2 flux are overestimated, and the likely source is in the experimental estimates of convective O-2 transport at upstream and downstream points of unbranched vascular segments.
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