Plasma and aortic lipids in experimental canine atherosclerosis

Abstract

Twenty-four dogs were split into three equal groups for an experimental period of 1 year. Group A was fed a semisynthetic diet containing 5% cholesterol and 16% hydrogenated coconut oil (HCO). Another eight dogs were fed diet B which differed from diet A only in that one-quarter of the HCO was replaced by safflower oil. Group C ate a controlled diet of meat and kibble. Diet A contained no essential fatty acids while diets B and C contained sufficient amounts of linoleic acid to satisfy established nutritional requirements. Severe aortic, coronary, and cerebral atherosclerosis was present at autopsy in group A dogs but no lesions were observed in any of the dogs fed diets B and C. All dogs of group A had profound elevations in plasma lipid concentrations when compared with dogs of control group C. Dogs of group B had more moderate increases. The largest elevation occurred in the cholesteryl esters of group A. The predominant ester in the plasma of group A dogs was cholesteryl oleate. In contrast, the major plasma cholesteryl ester in dogs of groups B and C was linoleate. Intima-media samples from atherosclerotic aortic segments showed large increases in lipid concentrations. The bulk of the increases was due to the accumulation of cholesteryl esters and the major cholesteryl ester within the lesion was oleate. The predominant cholesteryl ester in the normal intima-media of groups B and C was cholesteryl linoleate. Fatty acid analyses suggested that much of the lesion cholesteryl ester could have been derived directly from plasma, but the preferential accumulation of cholesteryl oleate and eicosatrienoate suggested that there was also considerable local cholesteryl ester synthesis. Phospholipid eicosatrienoate:arachidonate ratios in excess of 0.4, indicative of essential fatty acid deficiency, were found consistently in the plasma and aortic tissue of group A dogs but not in dogs of group B or C. Essential fatty acid deficiency appeared to be most severe within atherosclerotic intimal plaques.