PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “ARTERIOSCLEROSIS/experimental”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMed1958

Blood pressure, cholesterol content of serum and tissues and atherogenesis in the rat.

Rats on a stock diet with added cholesterol, cholic acid, and thiouracil developed increased concentrations of cholesterol, total lipide, and beta lipoprotein in the serum, and an increased content of cholesterol in the liver and carcass, despite the fact that the diet produced a cessation of endogenous cholesterol synthesis. Rats with high serum lipide concentrations developed intimal lesions similar to those of human atherosclerosis. The induction of hypertension by desoxycorticosterone and salt accelerated the development of hypercholesterolemia, hyperlipemia, increase in tissue cholesterol content, and atherosclerotic changes in the intima. Hypertension induced by renal artery constriction also intensified the hypercholesterolemia and hyperlipemia. On the other hand, rats receiving desoxycorticosterone acetate without salt or salt without desoxycorticosterone acetate did not show any intensification of hypercholesterolemia or hyperlipemia. The extent of the atherosclerotic lesions was correlated with the concentration of cholesterol in the serum. There was also a positive correlation between blood pressure and the degree of hypercholesterolemia. It remained uncertain whether the increase in atherosclerosis in the hypertensive animals was dependent on the increased lipide content of serum and tissues or on a local effect of the elevated blood pressure.

Animals↗
PubMed1959

Experimental atherosclerosis and cardiac infarcts in rats.

Marked obesity was induced in rats by feeding a high fat, egg yolk-rich diet. The obese rats were hyperlipemic and showed an increased incidence of lipomatous coronary lesions, but did not develop severe atheromatous lesions. Spontaneous vascular lesions of several kinds have been observed in aging rats. Among them, plaques containing a fibrin-like material seem to be conspicuous. However, these lesions differ from the experimentally induced changes, which were more fatty. Atherosclerosis, as it is defined in human pathology, has not been observed to develop spontaneously in rats. Experimental induction of marked hyperlipemia and hypercholesterolemia by feeding a high fat egg yolk-rich diet (supplemented with cholesterol, choleate, and thiouracil), and use of viosterol to cause vascular injury, led to severe atherosclerosis, coronary occlusion, and myocardial infarction. A consideration of all the findings reported here leads to renewed support of the concept that atherosclerosis has a combination of causes (Aschoff, Anitschkow, Page). Of all the etiological factors considered here, elevation of blood lipides and vascular injury are thought to be the most important ones.

Animals↗
PubMed1961

Triton hyperlipemia in dogs. II. Atheroscieross, diffuse lipidosis, and deletion of fat stores produced by prolonged administration of the non-tonic surface-active agent.

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.

Animals↗
PubMed1952

The effects of cholesterol dosage, cortisone, and DCA on total serum cholesterol, lipoproteins, and atherosclerosis in the rabbit.

The effects of cholesterol dosage, cortisone, and desoxycorticosterone acetate on total serum cholesterol, lipoproteins, and atherosclerosis were studied over a period of 112 days in thirty-two rabbits. Cholesterol was administered by feeding the rabbits diets containing 0.063, 0.25, and 1.0 per cent cholesterol At intervals measurements were made of total serum cholesterol and of low density lipid and lipoprotein components of three classes, S(f), 5-9, S(f) 10-15, and S(f) 16-30. All three classes of lipoproteins increased with cholesterol feeding. The total serum cholesterol concentration was linearly related to both the quantity of cholesterol consumed and its concentration in the diet. Lipoprotein and total serum cholesterol concentrations were significantly and equally well correlated with the severity of atherosclerosis. Cortisone administration in the normal rabbit increased the concentrations of total cholesterol and of lipoprotein components of the S(f) 10-15 and S(f) 16-30 classes, but did not produce atherosclerosis. Cortisone treatment in cholesterol-fed rabbits did not significantly affect the levels of serum lipoproteins, cholesterol concentration, or atherosclerosis produced by a 1.0 per cent cholesterol diet alone. Values for total cholesterol and S(f) 5-9 class of lipoproteins in DCA-treated animals were lower than those in controls but the degree of atherosclerosis was not significantly less.

Animals↗
PubMed1953

Experimental atherosclerosis in Cebus monkeys.

Atherosclerosis has been produced in Cebus monkeys by dietary means. This disease has been produced by feeding diets high in cholesterol and low in sulfur amino acids over periods of 18 to 30 weeks. Within 2 to 8 weeks this regimen caused the concentration of cholesterol in the serum to rise to 300 to 800 mg. per cent. The hypercholesterolemia could be largely prevented by feeding 1 gm. per day of dl-methionine or l-cystine as supplements to the diet. After the serum concentration had become elevated, it could be restored to normal by feeding 1 gm. of dl-methionine but only partially restored by 0.5 gm. of l-cystine daily. The vascular lesions were in the ascending aorta but extended from the valves of the left ventricle to the proximal portions of the carotid and femoral arteries. Minimal lesions have been observed in the coronary arteries. The aortic lesions were chiefly characterized by the presence of lipid-laden phagocytes and increase in collagen and elastic fibers. The lipids were in part cholesterol derivatives. Visceral cholesterolosis was not associated with this disease.

Animals↗
PubMed1954

The mechanism of alloxan protection in experimental atherosclerosis.

Experiments were performed to compare the effects of cholesterol feeding in (a) control rabbits, (b) alloxan-diabetic rabbits, and (c) rabbits injected with alloxan while the pancreas was temporarily occluded from the circulation. The alloxan-diabetic rabbits consumed significantly higher quantities of cholesterol and food and had serum cholesterol and lipoprotein (S(f) 5-9 and S(f) 16-30) concentrations significantly increased over the control levels. They failed to show a commensurate increase in the degree of atherosclerosis. Rabbits in which the diabetogenic action of alloxan was prevented by temporary occlusion of the pancreas from the circulation during its administration developed grades of hypercholesterolemia, hyperlipoproteinemia, and atherosclerosis not significantly different from the controls. The results are interpreted as indicating that the effects of alloxan on tissues other than the pancreas do not protect against experimental atherosclerosis produced by cholesterol feeding.

Alloxan↗
PubMed1954

The effect of undernutrition on cholesterol atherosclerosis in the rabbit.

Experiments were done to determine whether undernutrition with consequent loss of weight or failure to gain weight inhibited the development or promoted the regression of the aortic lesions of experimental cholesterol atherosclerosis in the rabbit. The experiments were conducted in such a way as to determine whether undernourished and adequately nourished rabbits fed the same daily doses of cholesterol would manifest different degrees of atherosclerosis at the end of an experiment. Different experiments tested the effect of undernutrition in young, growing animals that failed to gain weight normally (Experiments 1 and 2); in young rabbits subjected to marked undernutrition both before and during cholesterol feeding (Experiment 3); in fully grown, mature rabbits that lost weight during undernutrition (Experiment 4); and in rabbits that had completed a period of cholesterol feeding before caloric restriction was begun (Experiment 5). In every experiment it was observed that, if two groups of rabbits were fed cholesterol, one group being subjected to caloric restriction while the other received an adequate diet, no difference in aortic atherosclerosis was observed between the two groups at the termination of the experiment. Furthermore, no obvious effect of undernutrition on the regression of atherosclerotic lesions was observed in the rabbit. At the same time, undernutrition was found to promote hypercholesterolemia in the rabbit fed cholesterol. The possible significance of this result was discussed.

Animals↗
PubMed1954

The effect of cortisone on the serum lipids and on the development of experimental cholesterol atherosclerosis in the rabbit.

An experiment was performed to determine the effect of cortisone on the serum lipids and on the development of experimental cholesterol atherosclerosis in the rabbit. Litter mate rabbits of the same sex were employed; both sexes were represented in the experiment. The report is based upon four experimental groups comprising (1) 12 rabbits fed cholesterol and treated with cortisone vehicle; (2) 12 rabbits fed cholesterol and treated daily with cortisone; (3) 11 rabbits treated with cortisone; and (4) 7 rabbits that received cortisone vehicle. It was observed that: (1) There was less aortic atherosclerosis in the cholesterol-fed cortisone-treated rabbits as judged by both morphological and chemical means than in the rabbits fed cholesterol without cortisone treatment. (2) Cortisone depressed appreciably the hypercholesterolemia resulting from the feeding of cholesterol to rabbits. (3) Cortisone treatment caused a moderate hypercholesterolemia in normal rabbits. (4) Cortisone caused a moderate increase in serum lipid phosphorus equal to that produced by cholesterol feeding alone. (5) The combination of cholesterol feeding and cortisone did not result in a higher phospholipidemia than either one of these agents alone. (6) Cortisone caused a great increase in serum-neutral fat; it was not apparent whether cholesterol feeding affected the neutral fat lipemia due to cortisone treatment alone. (7) The total cholesterol to lipid phosphorus ratio was about normal in the rabbits that received cortisone only. It was doubled in the animals receiving both cholesterol and cortisone, and it was increased about four times in those that received only cholesterol. The significance of the alterations in the serum lipids induced by cortisone is discussed in relation to the inhibition of the development of aortic atherosclerosis that occurred in the cholesterol-fed rabbits treated with cortisone.

Animals↗