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We studied the effects of β-migrating very low density lipoprotein (β-VLDL) on the vascular responses of isolated thoracic aortic preparations taken from normal and hypercholesterolemic rabbits. The endothelium-dependent relaxation induced by acetylcholine or adenosine triphosphate (ATP) was attenuated in the arteries from hypercholesterolemic rabbits that were fed a cholesterol-rich diet for 12 weeks. In these aortas, the lesional circumference of the atherosclerotic plaques (fatty streaks) was only 12.18 ± 1.98 %. The relaxation induced by the Ca²⁺ ionophore A23187 or nitroglycerin was not altered. Preincubation with β-VLDL significantly inhibited the relaxation due to acetylcholine, ATP, or A23187, especially in the aortas of hypercholesterolemic rabbits. However, β-VLDL did not alter the response to nitroglycerin. Preincubation with high density lipoprotein had no significant effect on vessel relaxation. These results indicated that endothelium-dependent relaxation was already inhibited in the early stages of atherosclerosis, and that the atherogenic lipoprotein, β -VLDL, further inhibited endothelium-dependent relaxation in atherosclerotic aortas. It may be that β -VLDL also plays a role in determining the level of vascular tonus in atherosclerosis.

SummaryBy using a newly developed assay method for lipid peroxides based on their reaction with a leucomethylene blue derivative, we investigated serum lipid peroxides (LPO) in healthy and in diseased subjects. In 116 healthy subjects, the mean LPO level obtained was 1.45± 1.37 nmol/ml and showed significant correlations with total bilirubin, direct bilirubin, phospholipid, total cholesterol, high density lipoprotein-cholesterol, and low density lipoprotein-cholesterol. In 12 hypertensive patients, the LPO value was significantly higher (2.60±2.08 nmol/ml) compared with the healthy control, and LPO showed a significant correlation with serum globulin. In 16 hyperlipidemic subjects, the value was 1.50---0.86 nmol/ml and correlated with fibrinogen, white blood cells, and nonesterified fatty acids. In 19 diabetics, the level was not significantly different with that in the healthy control, and correlated with fasting blood sugar, total protein, and urea nitrogen. In 10 patients with liver dysfunction, LPO was 1.60±1.33 nmol/ml and correlated with white blood cells, chloride, and nonesterified fatty acids.

By the method using a methylene blue derivative, we investigated the hydroperoxide (LPO) level of erythrocyte membranes (EG) in patients suffering from diabetes mellitus, hypertension, cerebral stroke, hypercholesterolemia, and ischemic heart disease. In addition, the correlation between the EG-LPO level and the clinical parameters was analyzed. The EG-LPO level registered 1.6 ±0.9 nmol/mg protein in the healthy controls, whereas higher EG-LPO levels were obtained in the diabetic and the hypertensive patients. However, the EG-LPO in the hypercholesterolemic patients showed lower value than that in the diabetic, from which we would suggest the inhibitory effect of high cholesterol on lipid peroxidation. There was no correlation between the EG-LPO level and the clinical parameters. The lipid peroxide in the erythrocyte membrane would be supposed to be one of the independent vascular risk factors, and especially the high values of the EG-LPO in the diabetic and hypertensive patients might be related to the high incidence of vascular accidents in these diseases.