A theoretical study of mass transfer between tissue and blood at the apex of a branched blood vessel

Abstract

Simplified model of diffusion of inflammatory products, controlled by shear dependent permeability of the endothelium, is proposed to account for the localisation of a medial gap (caused by tissue breakdown) at a bifurcation apex, the endothelial barrier being intact at this stage. For the later stage where the artery wall is broken, a diffusion boundary layer model is proposed which predicts that, in a particular case, the diffusion flux through the break is about 400 times larger than the flux which would exist if the wall was intact at that point, and at least 40 times the down-stream flux for a shear stress of 300 dynes/cm2.