The feeding of egg yolk or pure cholesterol to rabbits produces an abundant deposit of anisotropic fat in various organs. From this deposit characteristic lesions secondarily result in certain organs. Prominent among these lesions is an atheroma of the aorta very similar in the gross and histologically to the human lesion. Lesions of other vessels are also produced, conspicuous among which are those of the branches of the pulmonary artery. There is a large deposit of anisotropic fat in the liver which produces a cirrhosis. Enlargement of the adrenals occurs, probably due to the storage of an excessive amount of anisotropic fat. In a certain proportion of rabbits conspicuous lesions are produced in the kidneys consisting of nodular deposits of anisotropic fat in the medullary portion, the fat being contained for the most part in endothelial cells and fibroblasts in the interstitial tissue. Later softening occurs in these areas as in the aorta; the cells break down; there is an abundant deposit of cholesterol crystals, some calcification, and a proliferation of connective tissue. Scars frequently extend outward from these lesions through the cortex, but the nodular deposits of anisotropic fat are never seen in the cortex. It is impossible to determine definitely from these experiments whether or not these deposits are dependent on preexisting interstitial lesions.
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1 January 1916
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January 01 1916
ATHEROMA AND OTHER LESIONS PRODUCED IN RABBITS BY CHOLESTEROL FEEDING
C. H. Bailey
C. H. Bailey
From the Pathological Laboratory of the Medical School of Leland Stanford Junior University, San Francisco.
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C. H. Bailey
From the Pathological Laboratory of the Medical School of Leland Stanford Junior University, San Francisco.
Received:
July 08 1915
Online ISSN: 1540-9538
Print ISSN: 0022-1007
Copyright, 1916, by The Rockefeller Institute for Medical Research New York
1916
J Exp Med (1916) 23 (1): 69–84.
Article history
Received:
July 08 1915
Citation
C. H. Bailey; ATHEROMA AND OTHER LESIONS PRODUCED IN RABBITS BY CHOLESTEROL FEEDING . J Exp Med 1 January 1916; 23 (1): 69–84. doi: https://doi.org/10.1084/jem.23.1.69
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