Rat basal resistance level under stress and nonstress conditions.
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Biomedical subjects
Publications and source records attributed to R KAPLAN.
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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.
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The intravenous injection of rabbit antidog-placenta or antidog-kidney serum produced immediate evidence of glomerulonephritis in dogs. The lesions produced by the two agents were indistinguishable. The glomerulonephritis so induced may terminate in death within 8 days, may progress to a chronic form or may heal. The acute phase of the nephritis was usually associated with severe exudative and necrotizing renal lesions, while the pathologic sequences in surviving dogs were essentially reparative. However, 1 dog of 8 in the chronic phase developed a progressive chronic nephritis and died in uremia.
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