Gross Endothelial Layer Blistering and Vascular Injury

Abstract

In 1856 Virchow proposed that injury to the vascular endothelium was the precipitating event which lead to the formation of an atherosclerotic plaque (1). Recently Ross and Harker (2) and others have demonstrated plaque like lesions in experimental animals following intentional endothelial layer desquamation. The siting of atherosclerotic lesions in humans has led investigators familiar with the laws of fluid mechanics to suspect that factors related to fluid flow influence the patterns and that through a careful study of arterial fluid mechanics a mechanism of arterial endothelial injury could be dicovered (3). Many mechanisms have been proposed: 1. Concentration polarization of macromolecules or platelets may occur due to ultra filtration across the artery wall; this would lead to injury at sites of low fluid shear rate. 2. Fluid shearing stress causes the endothelium to become more permeable to macromolecules; this would lead to injury at sites of high or fluctuating fluid shear rate (4). 3. Regions of low fluid hydrostatic pressure cause subendothelial fluid to accumulate at these sites; injury should be focused at local pressure minima (5). The agreement between observed frequency of plaque siting and the estimated site of a local pressure minimum is good (5).