Lipid Composition and Metabolism of Thromboatherosclerotic Lesions Produced by Continued Endothelial Damage in Normal Rabbits
Thromboatherosclerotic and fibrous lesions were produced by endothelial damage with polyethylene catheters inserted into the aortas in rabbits on a normal diet. Two weeks after insertion of the catheters, the concentration of both free cholesterol and cholesteryl ester in the thromboatherosclerotic lesions was significantly greater than that in the adjacent normal intima. A further increase in the concentration of free cholesterol and particularly of cholesteryl ester occurred during the remainder of the 4-month study period. Gas-liquid chromatography indicated that the raised thromboatherosclerotic lesions contained more cholesteryl oleate and less cholesteryl linoleate than did either the normal intima or the fibrous lesions. The incorporation of [1-14C] oleic acid into combined lipid in the aortas incubated in vitro showed that, by 2 weeks, two to three times more oleic acid had been incorporated into cholesteryl ester in the thromboatherosclerotic raised lesions than in the normal intima. A similar increase was demonstrated at 2 and 4 months. When [32P] phosphate was used as a precursor, incorporation into lecithin was higher and incorporation into phosphatidyl inositol was lower in the raised lesions than they were in the normal intima. Fibrous lesions did not differ significantly from the adjacent normal intima in their incorporation of either of these precursors into lipid. Therefore, the accumulation of cholesteryl ester in the thromboatherosclerotic lesions resulted in part from synthesis in the arterial wall, which was stimulated by the prominent platelet components of the lesions.
- arterial metabolism
- cholesterol arterial injury
- platelet thrombi
- cholesteryl ester
- Received October 9, 1973.
- Accepted January 10, 1974.
- © 1974 American Heart Association, Inc.