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Haemodynamically significant plaque formation and regional endothelial dysfunction in cholesterol-fed ApoE-/- mice

Journal article
Authors Maria E Johansson
Ulrika Hägg Samuelsson
Johannes Wikström
Anna Wickman
Göran Bergström
Li-Ming Gan
Published in Clinical Science
Volume 108
Issue 6
Pages 531-8
ISSN 0143-5221
Publication year 2005
Published at Cardiovascular Institute
Institute of Physiology and Pharmacology, Dept of Physiology
Pages 531-8
Language en
Keywords Acetylcholine/pharmacology, Animals, Aorta, Apolipoproteins E/*genetics, Arteries, Arteriosclerosis/*etiology/physiopathology/ultrasonography, Blood Pressure, Cholesterol, Dietary/*administration & dosage, Coronary Vessels/metabolism, Echocardiography, Doppler, Pulsed, Endothelium, Vascular/*physiopathology, Female, Image Processing, Computer-Assisted, Mice, Mice, Inbred C57BL, Mice, Knockout, Nitroprusside/pharmacology, Random Allocation, Vasodilator Agents/pharmacology
Subject categories Physiology


Flow-mediated vasodilation is suggested as one of the mechanisms involved in arterial expansive remodelling, which is thought to be a defence mechanism in atherogenesis. In the present study, we tested the hypothesis that lumen obstructive plaque formation is associated with failure of NO (nitric oxide)-dependent vasodilation in conduit vessels. Cardiac function and aortic root flow velocities were assessed using high-resolution echocardiography and two-dimensional-guided pulsed Doppler in ApoE(-/-) (apolipoprotein E-deficient) mice fed a standard or high-cholesterol diet. Endothelial function in the proximal and mid-descending aortic regions was studied using a myograph technique. Flow velocity at the aortic root of cholesterol-fed ApoE(-/-) mice was significantly increased as a result of lumen narrowing, detected via histological analysis. NO-dependent vasodilatory responses were selectively impaired in the atherosclerosis-prone vascular regions in cholesterol-fed ApoE(-/-) mice. In conclusion, consumption of a high-cholesterol diet results in lumen obstructive plaque formation in ApoE(-/-) mice, which significantly alters aortic root haemodynamics. This phenomenon is associated with impaired NO-dependent vasodilation in vessel segments known to be prone to atherosclerosis.

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