No abstract

The authors examined the effects of splenectomy on serum lipids in patients with hematologic disease, in rabbits, and also in cholesterol-fed rabbits with experimental atherosclerosis. Serum cholesterol was determined in patients with hypersplenism before and after splenectomy. Meanwhile serum lipids were determined in two groups of rabbits: splenectomy group (Spx group, n = 19), and sham operation group (Sham group, n = 14) before and after the operation. Then the rabbits were divided into four subgroups: cholesterol-fed groups--Spx-C (n = 12) and Sham-C (n = (9), and normal-chow-fed groups--Spx-N (n = 7) and Sham-N (n = 5). The Spx-C and the Sham-C rabbits were fed 1% cholesterol diet and the Spx-N and Sham-N rabbits were fed normal chow for twelve weeks. In patients preoperative serum cholesterol levels were low, and significant increase in serum cholesterol was observed following splenectomy. In rabbits, the Spx-C group showed significantly higher levels of serum cholesterol, triglycerides, and phospholipids in contrast to lower levels of high density lipoprotein cholesterol, as compared with the Sham-C group. The percentage of aortic plaque area in the Spx-C group tended to be higher than that in the Sham-C group. On the other hand, the Spx-N and the Sham-N group showed no difference in serum lipids during twelve weeks. The worsening of atherosclerosis in the Spx-C group was considered to be mainly due to an enhanced hyperlipidemia. Their results suggest a possible role of the spleen in lipid metabolism, in particular the existence of a splenic factor that can cause hypocholesterolemia in hyperplenism and can suppress hyperlipidemia.

We investigated the mechanisms by which corticosteroids affect atherosclerosis. Male New Zealand White rabbits were injected with 0.125 mg dexamethasone (n = 10) or vehicle (control group, n = 10). Both groups were fed a 1% cholesterol diet for 8 weeks. Although the dexamethasone-treated animals exhibited a greater degree of hvperlipidemia, they exhibited significantly less atherosclerotic plaque of the aortic surface than control animals (7.8% versus 47.2%). Immunofluorescence study of the aortic plaque specimens showed that dexamethasone administration reduced both macrophages and T lymphocytes. In vitro, dexamethasone suppressed the proliferation and differentiation of U937 cells and inhibited uptake and degradation of 0-very low density lipoproteins by mouse peritoneal macrophages. These findings suggest that dexamethasone suppresses the development of atherosclerosis in the aorta of rabbits by inhibiting recruitment and proliferation of macrophages and the formation of foam cells in plaques. {Arteriosclerosis and Thrombosis 1993;13:892-899)

No abstract

No abstract