Atherosclerosis following balloon catheter injury to the carotid artery and the aorta of hypertensive rats with normolipidemia or hyperlipidemia.

The carotid artery and abdominal aorta of hypertensive normocholesterolemic rats responded in similar manner to balloon denuding of the endothelium. One denuding resulted in an intimal fibrous plaque, while multiple such injuries increased the lipid content of the plaque and so yielded fatty-fibrous plaques, which perhaps represent an intermediate stage of atherosclerosis. In no instance did a single or multiple denuding lead to advanced atherosclerosis.

Regression of atherosclerotic plaques in rhesus monkeys. Angiographic, morphologic, and angiochemical changes.

On a diet with high levels of cholesterol and sucrose, a beta-lipoproteinemia developed in rhesus monkeys that is similar to type II human hyperlipidemia. Lesion regression appeared in response to drastic lowering of serum cholesterol (SC) levels. This experiment analyzed angiochemical responses on the addition of a bile-acid sequestrant to continued atherogenic feeding, which resulted in ranges of moderate cholesterolemia that mimick those that occur in man.

Arterial wall renin and renal venous renin in the hypertensive rat.

1. Infusion of sufficient renin to raise the blood pressure of normal rats to hypertensive levels resulted in increased renin in the arterial wall. 2.

Failure of regression of atherosclerosis in dogs with moderate cholesterolemia.

Controversy exists as to whether regression occurs in atherosclerotic plaques in response to serum cholesterol reduction. In the present study, using sequential observation of canine atherosclerosis, we attempted regression in hypothyroid dogs. Animals with established lesions prior to a regression attempt were placed on a 0.

Effect of caloric restriction on basal insulin levels and the in vivo lipogenesis and glycogen synthesis from glucose in the Koletsky obese rat.

Fasting plasma immunoreactive insulin levels increased with age in hyperinsulinemic Koletsky obese rats, being almost four times as high as in lean siblings at 3 mo (40 +/- 5 muU/ml) and rising steadily to 82 +/- 4 muU/ml at 6 mo (about seven times higher than lean siblings). Restricting the food intake of the obese rats markedly reduced but did not normalize the hyperinsulinemia, which in these rats was accompanied by normal plasma glucose concentrations. The incorporation in vivo of D-U-14C-glucose into tissue lipids and glycogen was measured 1 hr after the intravenous injection of 1 g glucose (containing 100 muDi D-U-14C-glucose) per kg body weight in obese rats eating ad libitum, obese rats after 3 mo on a restricted food intake, and lean siblings.

Simultaneous determination of plasma aldosterone, corticosterone, 11-deoxycorticosterone, 18-hydroxydeoxycorticosterone, cortisol, and 11-deoxycortisol. Methods and applications.

A method for the simultaneous determination of aldosterone, corticosterone (B), 11-deoxycorticosterone (DOC), 18-hydroxy-11-deoxycorticosterone (18-OH-DOC), cortisol, and 11-deoxycortisol in a single 1-ml sample of plasma is described. The method is applicable to both man and experimental animal. After extraction and purification by thin-layer chromatography (TLC), aldosterone was determined by radioimmunoassay (RIA) employing antibodies to aldosterone: B, DOC, cortisol and 11-deoxycortisol were determined by RIA employing antibodies to corticosterone; 18-OH-DOC was obtained colorimetrically using the Porter-Silber reagent.

Effect of low calorie diet on the hyperlipidemia, hypertension, and life span of genetically obese rats.

A new strain of genetically obese rat recently obtained in our laboratory exhibits endogenous hyperlipidemia (marked hypertriglyceridemia and moderate hypercholesterolemia) and spontaneous hypertension. The animals die prematurely from kidney failure or from the complications of atherosclerosis. A low calorie diet proved to be highly beneficial to these rats.

Pathologic findings and laboratory data in a new strain of obese hypertensive rats.

A new strain of rat characterized by genetic obesity, endogenous hyperlipidemia, and hypertension was obtained in this laboratory. The abnormal phenotype is inherited as a homozygous recessive trait. The animals exhibit marked hypertriglyceridemia, moderate hypercholesterolemia, and an electrophoretic pattern resembling that of human Type IV hyperlipoproteinemia.