Abstract
The theoretical study of the subendothelial spread of macromolecules in the vicinity of a localized endothelial damage is of importance because of the large increased uptake of macromolecules which has been observed experimentally in certain regions of the arterial tree as compared to other regions. It has been hypothesized that the locally observed increased permeability may be due to endothelial injury produced by naturally occurring hemodynamic factors. The two-phase arterial wall model developed by Weinbaum & Caro (1976) has been extended to obtain analytic solutions for the time dependent and steady state concentration distributions, flux and uptake in the arterial wall as a function of damage size, fraction of damaged surface and position from the damage. It has been demonstrated that with as little as 3% of the endothelial., surface damaged with locally spread holes of size 0·1 the thickness of the arterial media, the total uptake can increase by a factor of 2·5 over that of an artery with no endothelial damage.
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