Sequential changes in the plasma lipids of rats injected with Triton were studied. It was observed that following a dose of Triton, the accumulation of triglyceride (neutral fat), cholesterol and phospholipid proceeded in plasma for about 36 hours, after which time a rapid diminution began. Excess triglyceride began both to accumulate and to disappear, respectively, before the other two substances. During the phase of accumulation, the excess cholesterol in plasma was not found to be reflected by any increase in cholesterol either in the liver tissue or in hepatic lymph. This lack of diffusibility of plasma cholesterol disappeared during the period of recovery. Injection of Triton retarded the escape of both injected triglyceride and phosphatide from the plasma of the liverless rat. Hypercholesteremia could be induced in the liverless rat by Triton injection if triglyceride, phosphatide or both were given with the Triton. It is suggested that the hypercholesteremia occurring after injection of Triton is due to the latter's ability to retain excess triglyceride and phospholipid which then in turn mobilizes and sequesters cholesterol from both extrahepatic and hepatic sources.
Pattern A appeared to be remarkably similar to men with Pattern A as regards the incidence and intensity of their blood and cardiovascular abnormalities.Since the dietary, physical activity and various other characteristics of these different types of individuals were approximately the same, we concluded that in some manner Behavior Pattern A itself was causally responsible for the altered lipid and clotting dynamics of the blood and for the clinical changes found. The question of how such a behavior pattern might induce such changes remained to be clarified. As a first attempt to ferret out possible clues, it was decided to study the urinary excretion of some possibly relevant hormones in groups of men exhibiting Behavior Pattern A or Pattern B. The results of this study are presented below. METHODSChoice of men and method of urine collection. In our earlier study (2) a large group of men had been chosen for us (by lay selectors) who exhibited either Behavior Pattern A or B. In our own personal interview, we also had the opportunity to judge for ourselves the intensity of the pattern present in each volunteer subject. We therefore selected 12 men (between the ages of 35 and 50 years) from each of these two groups who we believed possessed most completely the characteristics of the respective two behavior patterns.Earlier we expressed our belief (5) that Behavior Pattern A might be a resultant of the interplay between a provoking environment and a particular type of personality. We therefore employed three general criteria in selecting the 12 men of Group A. First, each of the 12 men occupied a position not necessarily of top executive quality but associated with or demanding extreme competitive activity and deadline preoccupations. Thus, of the 12 men selected, 4 were managing or city editors; 7 were corporation executives who were themselves 758
Earlier studies from this laboratory( 1.2) have demonstrated that a sustained rise in the plasma phospholipid of either the rat or rabbit, induced by intravenous infusion of a suitable mixture of phosphatides. quickly leads to a hypercholesteremia in these species. A third study(3) also demonstrated that this phosphatide-induced hypercholesteremia could occur almost as well in the liverless as in the intact animal. This last finding of course indicated that the infused phosphatide was bringing into the blood. cholesterol from parts of the body other than the liver.In view of these findings. it was thought advisable to determine whether a series of phosphatide infusions, administered to rabbits previously made hypercholesteremic and atherosclerotic by dietary ingestion of cholesterol, might alter the cholesterol content and extent of their aortic atherosclerotic process.Methods. Two series of hypercholesteremic rabbits were studied. A very moderate hypercholesteremia was induced in the first series of 10 healthy male rabbits (avg age: 6 weeks; appx wt: 1500-1800 g) by placing them on Purina rabbit chow, containing 1% cholesterol and 270 cottonseed oil, for a period of 3 months. A very severe hypercholesteremia was induced in the second series of 14 rabbits by adding 3% cholesterol and 4% cottonseed oil to their Purina rabbit chow for a period of 3 months. At the end of this period, both series were returned to their regular rabbit chow diet. Plasma samples were taken before and then monthly after the high cholesterol feeding had been begun and analyzed for cholesterol ( 4 ) . Monthly plasma samples also were obtained after the diet had been discontinued. Three months after cessation of excess cholesterol and oil feeding, the hypercholesteremia observed during the * .4ided by grants irom Liie Insurance Medical Research Fund, S a t . Heart Inst., Alameda County Heart A s h . and Sterling-Winthrop Research Inst. __--cholesterol feeding had disappeared. At this time. for control purposes, 4 rabbits of the second series were sacrificed and their aortas were examined for gross atherosclerosis and a segment of it was analyzed for cholesterol. This segment (1 cm in length) was taken a t a site uniformly 3 cm distant from the semilunar valves. For additional controls, the aortas of 5 completely normal rabbits were analyzed for total cholesterol content. The average plasma cholesterol of the remaining rabbits of both series was calculated for only the period of high cholesterol feeding by averaging the 4 samples obtained just prior to, and for 3 successive months, respectively, while they were on the special diet. These latter values then were employed to divide the rabbits of each series into pairs, of which each member had approximately the same degree of previous hypercholesteremia. After this was done, a plastic cannula (external diameter: 1.5 mm) was inserted under ether anesthesia into the external jugular vein of each rabbit. The catheter then was filled with saline, temporarily sealed a t its open end and. by tunnel...
Injection of triton WR-1339 into rats leads to a rapid increase in the cholesterol, cholate, and various lipid fractions of their blood. The increase in cholesterol is confined to the blood itself. The cholesteremic effect of triton was not dependent upon a prior accumulation of cholate in plasma. The liver was found to be the source of the excess cholesterol but the rate of cholesterol synthesis, the excretion of cholate, and the cholesterol content of the liver were not changed by injection of triton. The cholesteremic effect of triton is not due to alteration in the intestinal excretion of cholesterol. Transfer of blood between "tritonized" and normal rats leads to a disappearance of the hypercholesteremia in the former and its appearance in the latter animals. The plasma proteins of rats injected with triton are markedly changed qualitatively. Heparin was found to inhibit the hypercholesteremic effect of triton. The hypercholesteremia following triton injection appears to be due to a fundamental physicochemical change in the plasma proteins produced by injection of this detergent.
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