TRITON HYPERLIPEMIA IN DOGS

Abstract

Fourteen dogs, fed a regular diet and given 250 mg/kg of triton (a non-ionic surface-active agent) intravenously every 4th day, exhibited a progressively severe hyperlipemia. Serum triglycerides were the first to increase. Cholesterol, mostly in the free form, and phospholipids showed elevation only at a later stage and increased at almost identical rates. The plasma-free fatty acid concentration was from 2 to 3 times above normal. With establishment of sustained hyperlipemia, there was reduction, followed by total disappearance, of the high density D 1.063 to 1.21 lipoprotein. Most of the cholesterol and phospholipids (70 to 75 per cent of the total) were found in the D 1.006 to 1.063 lipoprotein class, the remainder in the D < 1.006 class. Triglycerides were almost evenly distributed between these two classes. The concentration of the serum lipoprotein proteins was within normal limits. All of the animals died within from 4 to 5 months after receiving the first injection of triton. Autopsy findings consistently showed: (a) numerous lipidladen macrophages in the liver, spleen, and lymph nodes; (b) significant depletion of all fat stores; (c) presence of lipids, either free or engulfed in macrophages (foam cells), in the subintima of the coronary arteries, aorta, and pulmonary arteries, indicating an early stage of atherosclerosis. Concurrent daily administration of heparin (5 mg per kilogram of body weight) did not substantially change the course of the disease. Withdrawal of triton from animals that had been receiving the detergent for from 3 to 4 months, elicited a slow return to normal of the lipid pattern. In two dogs killed when normolipemia was reestablished, all tissues were normal with the minor exception of a few hepatic macrophages still laden with sudanophilic material. It is postulated that the primary action of the injected triton was on the lipid moieties of plasma lipoproteins with formation of complexes, which, as foreign bodies, were preferentially taken up by the cells of the reticuloendothelial system. Depletion of fat stores was probably secondary to increased lipid mobilization, as an attempt by these tissues to supply energy to the parenchymal cells unable to utilize triton-bound lipids.