The problem of diffusion of O-2 across the endothelial surface in precapill
ary 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 o
f published in vivo measurements. To interpret the data, we utilized a diff
usion model of the vascular wall and computed possible physiological ranges
for O-2 consumption. We found that many flux values were not consistent wi
th the diffusion model. We estimated the mitochondrial-based maximum O-2 co
nsumption of the vascular wall (M-mt) and a possible contribution to O-2 co
nsumption of nitric oxide production by endothelial cells (MNO). Many value
s of O-2 consumption predicted from the diffusion model exceeded M-mt + M-N
O. In contrast, reported values of O-2 consumption for endothelial and smoo
th 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 a
re overestimated, and the likely source is in the experimental estimates of
convective O-2 transport at upstream and downstream points of unbranched v
ascular segments.