Several hypotheses have been advanced as possible explanations for the effects of injury. One of these 8 is that removal of the endothelium eliminates a barrier to influx of macromolecules from plasma. Others 9 argue that the endothelium prevents efflux of macromolecules from the artery. At present, relatively few studies have considered the contribution of plasma cholesteryl ester influx to the observed excess cholesteryl ester accumulating in the artery This work was supported by Research Grant HL10933 from the National Heart, Lung and Blood Institute of the United States Public Health Service. Donald B. Zilversmit is a Career Investigator of the American Heart Association. Dawn C. Schwenke held a National Science Foundation Graduate Fellowship during these studies.Received April 17, 1986; revision accepted March 18, 1987. after injury. Most of the measurements of cholesteryl ester influx 3 or lipoprotein accumulation 1011 into previously injured areas of the arterial wall have been made at relatively long times (months) after injury. At these times, the composition of the arterial wall In both reendothelialized areas and those remaining deendothelialized is considerably altered compared with uninjured areas.2 ' 7 1 2 1 3 Several studies suggest that the atherosclerosis risk factors, hypercholesterolemia 14 ' 15 and hypertension, 16 injure the arterial endothelium.Other studies 10 have measured the ability of acutely deendothelialized arterial tissue to limit the accumulation of low density lipoprotein (LDL) in vivo. Yet others 17 have studied the uptake of LDL by perfused vessels. The present investigation addresses the question of whether removal of aortic endothelium and perhaps underlying elements affect cholesteryl ester accumulation primarily by reducing the barrier to influx or to efflux of cholesteryl ester, or both. Specifically we have asked: 1) Does injury to the luminal surface of the artery result in enhanced cholesteryl ester influx in the injured artery? 2) If cholesteryl ester influx is elevated in injured areas, does the cholesteryl ester content of these areas increase concomitantly with the enhanced influx? 3) Is cholesteryl ester turnover altered in injured areas?
Methods
ChemicalsAll chemicals were reagent grade. Cholesterol methyl ether, 99% pure, (A 5 -cholesten-3G-ol-36-methyl) was pur-