Uptake of 3H-7-cholesterol along the arterial wall at an area of stenosis.

Abnormal uptake of atherogenic substances and lipid infiltration have been believed to contribute to the localized genesis and development of atherosclerosis, as well as to late failures of synthetic arterial prostheses. To verify the theoretical prediction that accumulation of lipoproteins on the luminal surface of arterial walls occurs in the regions of disturbed flow, we have carried out an in vitro mass transfer experiment to test the effect of a pseudo steady recirculation flow on the uptake of 3H-7-cholesterol by the arterial wall at a surgically created stenosis. It was found that, as predicted by the theory, in the flow field of the stenosis the uptake of labeled cholesterol reached a maximum around the reattachment point of the vortex distal to the stenosis, where the wall shear stress was lowest (zero). This value of the highest uptake rate was almost twice the average, whereas the uptake level was at a minimum at the stenosis itself where the wall shear stress was highest. The lowest uptake was only 60% of the average. These results provide strong support to our hypothesis, based upon the theory that, in addition to the flow induced changes to the biologic function of endothelial cells, the disturbed flow with slow recirculation itself favors the accumulation of atherogenic lipoproteins at the blood-endothelium boundary, therefore playing an important role in the localized pathogenesis and development of atherosclerosis.