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LIPID DEPOSITION IN THE INJURED WALL OF THE CAROTID ARTERY IN THE HYPERCHOLESTEROLÆMIC AND HYPERLIPÆMIC RABBIT
Author(s) -
Courtice F. C.,
Schmidt-Diedrichs A.
Publication year - 1962
Publication title -
quarterly journal of experimental physiology and cognate medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.925
H-Index - 101
eISSN - 1469-445X
pISSN - 0033-5541
DOI - 10.1113/expphysiol.1962.sp001601
Subject(s) - internal elastic lamina , aorta , endothelium , lesion , cholesterol , arterial wall , saline , thickening , artery , foam cell , pathology , medicine , chemistry , endocrinology , anatomy , lipoprotein , polymer science
A portion of the inner wall of the carotid artery was injured by physiological saline at 55–60° C. for 30 sec. in four groups of rabbits, (i) on a normal diet; (ii) on a normal diet with intravenous infusions of Lipomul; (iii) on a normal diet with repeated Triton WR‐1339 injections to give a sustained hyperlipæmia; (iv) with cholesterol added to the diet to give a sustained hypercholesterolæmia. In the first two groups, injury caused a fibrocellular thickening of the intima with no lipid deposition 1 week or more after injury. The Lipomul particles did not penetrate the endothelium. In Triton hyperlipæmia and in hypercholesterolæmia, the injury immediately caused patchy extravasations of lipoprotein into the media, either localized just beneath the internal elastic lamina or involving most of the media. The permeability of the arterial endothelium to lipoproteins in each group after injury was similar to that in the capillaries of the leg. From 1 to 8 weeks after injury the intima in the injured area showed fibrocellular thickening in each case; but in the Tritonized group there was little or no lipid deposits whereas in the hypercholesterolæmic group the resulting lesion contained large amounts of lipid, partly intracellular, and resembled the atheromatous plaques found in the aorta after prolonged cholesterol‐feeding. The difference in these two groups appeared to be due not to any difference in permeability of the endothelium to lipoproteins, but to a difference in the ultimate fate of the lipoproteins in the arterial wall. The possible mechanisms are discussed.