Long-term ethanol consumption initiates atherosclerosis in rat aorta through inflammatory stress and endothelial dysfunction

Shirpoor, A and Salami, S and Khadem Ansari, M.H and Heshmatian, B and Ilkhanizadeh, B (2012) Long-term ethanol consumption initiates atherosclerosis in rat aorta through inflammatory stress and endothelial dysfunction. Vascular Pharmacology, 57 (2-4). pp. 72-77.

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Abstract

Controversy exists on whether alcohol has a direct cardioprotective effect or it provokes atherosclerosis, so the present study sought to assess the effect of chronic consumption of ethanol on the markers of endothelial function, vessel rigidity, and atherosclerosis in the aorta of rat. Male Wistar rats were selected randomly and exposed to ethanol (4.5 g⁄kg of 20% w/v solution in saline) once per day for 6 weeks. Blood pressure, hemodynamic parameters, foam cell formation, intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial-leukocyte adhesion molecule-1, and high-sensitivity C-reactive protein (CRP) were assessed in ethanol treated rats and compared with either sham or control rats. The results revealed a concurrent significant increase of adhesion molecules, CRP levels, systolic, diastolic, pulse, and dicrotic pressures as well as enhanced formation of foam cell in ethanol-treated rats. These findings implicate that long-term ethanol exposure provokes atherogenic and hemodynamic changes via significant induction of proinflammatory response, augmenting of cell adhesion molecules, stiffness in rat aorta wall and induction of foam cell formation.

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