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Biomedical subjects

L Levy

Publications and source records attributed to L Levy.

At least 271 records · Page 15Linked to original sources
PubMed1970

Further studies on the reversibility of serum sickness cholesterol-induced atherosclerosis.

Rabbits were induced to form atheromatous cardiovascular lesions by subjecting them to treatments of a single BSA injection plus a 2-wk period of cholesterol diet, or to the diet alone. Microscopic examination of the hearts at the end of the 2-wk induction period, or after having been returned to regular diet for 5 or 8 wk, showed that lesion incidence in the cholesterol-only animall decreased markedly during the 8-wk rest period, while little change in incidence occurred in animals with lesions from the combined treatment. This finding was taken to mean that the latter type of lesion was less reversible, and therefore perhaps more pathologically significant, than the former type. It was felt that lipid deposition was not solely responsible for this prolongation, since it was present in diet-only lesions which disappeared with time, and also seemed to be disappearing from the prolonged lesions in all treatment groups. On the other hand, elastic tissue was demonstrated only in lesions arising from the combined treatment, and it is hypothesized that this feature is implicated in the prolongation of these lesions.

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PubMed1968

Effect of removal of cholesterol diet upon serum sickness-cholesterol-induced atherosclerosis.

In this report, the role of vascular allergy (i.e., hypersensitivity) in the potentiation of atherogenesis has been studied. In order to accomplish this, bovine serum albumin (BSA) was administered to rabbits in quantities sufficient to cause the occurrence of serum sickness (a type of hypersensitivity known to cause injury to the endothelial linings of certain blood vessels). This was immediately followed by the feeding of a special cholesterol-supplemented diet, which is known to be capable of initiating a high incidence of atheromatous disease in rabbits after prolonged feeding. Results indicated that those animals which received the combined treatment developed an incidence of pathology after only 2 wk of special diet which was not equaled in the diet-only control groups until they had been treated for 4 wk. This indicated that vascular allergy could potentiate lipemia-induced atherogenesis in the rabbit, and was in confirmation of an earlier study of a similar nature. Indeed, because of the relatively mild vascular injury caused by a single injection of BSA, it would seem as though vascular hypersensitivity was extremely effective in the potentiation of atherogenesis. In addition, these results may have given some indication of the degree of vascular injury necessary for the induction of irreversible atheromatous disease. While the incidence of lesions in serum sickness controls was seen to decrease with passage of time after BSA challenge, it appeared to increase after cessation of treatment in those animals which received the combined treatment of BSA plus 2 wk of cholesterol-supplemented diet. It would therefore appear that the atheromatous lesions seen as early as 2 wk after initiation of the experiment may already have been irreversible in terms of the resolution of established pathology.

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