Abstract

These studies examine the hypothesis that removal of aortic endothelium eliminates a barrier to lipoprotein cholesterol influx. The aortas of rabbits fed a cholesterol-rich diet from 7 to 16 days before balloon injury were studied 1 or 2 days after deendothelialization of specific areas of the aorta. By this design the aortic sterol content was near normal on the day of injury, but areas of injured and noninjured aorta were exposed to identical levels of elevated plasma cholesterol. Measuring the arterial [ 3H]- and [ 14C] cholesterol fractions accumulated during 2 different intervals after dosage in the same animals permitted calculation of total influx and fractional loss of aortic cholesterol. During the first 2 days after deendothelialization, total (unidirectional) cholesteryl ester influx in deendothelialized aorta was similar to that in adjacent uninjured aorta, but total influx of nonesterified cholesterol was increased. The calculated increase in influx of nonesterified cholesterol was not a result of an increase in hydrolysis of entered cholesteryl ester but probably represents increased exchange of labeled cholesterol between artery and plasma. These results suggest that subendothelial layers of the aorta of short-term cholesterol-fed rabbits function as significant barriers to lipoprotein influx and that processes other than increased permeation by lipoproteins initiate injury-induced lesions.

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