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 55 records · Page 3Linked to original sources

The effect of alloxan diabetes on experimental cholesterol atherosclerosis in the rabbit. IV. The effect of insulin therapy on the inhibition of atherosclerosis in the alloxan-diabetic rabbit.

Experiments were undertaken to ascertain whether the previously demonstrated inhibition of the development of experimental aortic atherosclerosis in alloxan-diabetic rabbits fed cholesterol was due to the injection of alloxan per se or to the existence of the diabetic state produced by alloxan. It was established that, by treating the diabetic state with insulin, the diabetic state could be ameliorated and the inhibitory effect obviated. It was therefore concluded that the inhibitory phenomenon was not due to the injection of alloxan per se but that it was associated with one or more factors that characterize the alloxan diabetic state in the rabbit and that are reversible by insulin therapy. In the course of the experiment it was demonstrated that the inhibitory effect was apparent in cholesterol-fed diabetic rabbits whether or not their diet was supplemented with vegetable oil. The previously reported metabolic abnormalities of the diabetic animals were confirmed. It was established that suitable treatment of the cholesterol-fed diabetic animals with insulin would bring all the metabolic aberrations, including those of the serum lipids, into reasonably close correspondence with those observed in non-diabetic rabbits fed cholesterol.

Alloxan↗

The influence of anticoagulants on the formation and regression of experimental atherosclerosis.

The prolonged administration of either heparin or dicoumerol has been demonstrated to be effective in retarding the formation of atheromata in the cholesterol-fed chick. This beneficial action is possibly produced as a result of a demonstrated antihypercholesteremic action exerted by these anticoagulants. Heparin is ineffective in preventing the marked turbidity of sera from cholesterol-fed chickens. After the formation of atherosclerosis in the chick neither heparin nor dicoumerol is effective in hastening the regression of this condition. The serum lipid picture as well as the degree of atheroma of the various groups in the regression experiments is unaffected by the anticoagulants.

Anticoagulants↗

Does the ingestion of alcohol influence the development of arteriosclerosis in fowls?

The effect of alcohol ingestion upon the development of naturally occurring and stilbestrol-induced arteriosclerosis was studied in the domestic fowl. In two experiments, a 15 per cent ethyl alcohol solution was used for drinking purposes, and in a third experiment wine containing 12 per cent of it was administered. The caloric intake of both food and alcohol was carefully controlled by pair-feeding, a glucose solution being used for drinking purposes to equalize the caloric intakes of the control birds with those of the alcohol-treated birds. A total of 224 cockrels was studied, and the period of observation for each experiment lasted 12 months. The degree of arteriosclerosis in the thoracic and abdominal aortas was determined in the gross and microscopically, and the degree of lipide infiltration was determined microscopically. The gross grading of arteriosclerotic lesions agreed closely with the microscopic analysis of intimal thickening and lipide infiltration of the arterial wall. The gross gradings were subjected to a critical statistical analysis which allowed precise statements to be made on the probability that a real effect would be overlooked. This analysis yielded no evidence that alcohol or the wine used had affected the degree of gross arteriosclerosis or lipide infiltration.

Alcohol Drinking↗

Experimental production of gross atherosclerosis in the rat.

Gross atherosclerosis was produced in the rat by feeding purified diets containing cholesterol, sodium cholate, and thiouracil for periods up to 363 days. In a few weeks a marked increase of the serum cholesterol and beta lipoproteins as well as of the liver lipides was observed. Lesions visible in the gross were found on the intimal surfaces of the vessels of all 46 animals examined. These were most prominent in the heart valves and aortic arch. The earliest lesions, which were seen at 31 days, required Sudan staining for gross demonstration. Older lesions were visible without staining. Microscopic coronary artery lesions were present and in one instance were accompanied by massive myocardial infarction. Vascular lesions were characterized by medial and intimal lipide infiltration and cellular intimal plaque formation. In a part of this study the protein level of the diet was altered at the expense of sucrose. The hypercholesteremic response among the rats varied according to the dietary protein level. The lowest response was observed among those animals receiving the highest level of dietary protein. A difference, however, in the severity and extent of the arterial lesions among these relatively small groups of rats could not be established under these experimental conditions. In all these experiments a close correlation existed between the serum cholesterol levels and beta lipoproteins of the S(f)20-100 range.

Animals↗

Interrelationships between experimental hypercholesteremia, magnesium requirement, and experimental atherosclerosis.

The addition of cholesterol and cholic acid to a diet containing 24 mg. percent of magnesium, an amount normally required for young rats, resulted in magnesium deficiency in rats. This was characterized by hyperexcitability, hyperemia of the ears, calcium deposition in the kidney tubules, low serum magnesium levels, and decreased oxidative phosphorylation of heart mitochondria. All these lesions were prevented by raising the dietary magnesium level four to eight times. Feeding the atherogenic diet produced the deposition of lipide in the aorta and in the heart valves. The extent of this intimal sudanophilia was reduced by large amounts of dietary magnesium although serum cholesterol values did not fall and usually rose. This represents perhaps the first clear cut disassociation between serum cholesterol values and the extent of intimal sudanophilia. Raising the level of dietary protein from 10 to 20 per cent decreased the serum cholesterol levels and the extent of the kidney lesions. Thyroxine administration lowered the serum cholesterol values, abolished the kidney lesions and reduced the intimal sudanophilia. These effects occurred even though the serum magnesium levels remained low.

Animals↗