Diffusion of macromolecules across the arterial wall in the presence of multiple endothelial injuries.
In this paper, the two-phase arterial wall model developed by Weinbaum and Caro [2] has been extended to obtain analytic solutions for the steady-state flux, uptake and concentration of macromolecules in the arterial wall due to the presence of periodically dispersed local sites of enhanced permeability. In the endothelial cell layer these sites are believed to be associated with the dying and regeneration of individual cells in the endothelial monolayer. Nir and Pfeffer [9] obtained similar solutions for a single dying cell in an otherwise undamaged endothelial cell layer. However this model requires that multiple cell turnover sites be spaced sufficiently far apart such that no interaction between neighboring sites takes place and hence cannot be applied to closely spaced endothelial injuries which have been observed experimentally in physiological studies. The theoretical predictions of the present model compare very favorably with experimental results for the enhanced uptake found in blue versus white areas reported in morphological studies of the endothelial surface (Bell, et al. [10, 11]).
D000818:Animals; D001158:Arteries / Q000293:injuries / Q000378:metabolism*; D001692:Biological Transport; D004727:Endothelium / Q000166:cytology / Q000378:metabolism; D008954:Models, Biological; D010316:Particle Size; D010539:Permeability; D013552:Swine