Long-term ethanol consumption triggers atherosclerosis in rat aorta by inflammatory stress and endothelial dysfunction

alireza shirpoor1, Mohammad Hassan Khadem-Ansari0,2, Behnam Heshmatian1. 1Faculty of medicine, Physiology, Iran, 2Faculty of medicine, Biochemistery, Iran

Aims Growing evidence suggests that impaired endothelial function plays an important role in the primum movens of atherosclerosis, but the precise mechanism of ethanol-induced endothelial dysfunction and subsequent atherosclerosis has remained obscure. The present study sought to assess the effect of ethanol on the markers of endothelial function, vessel rigidity, and atherosclerosis in aorta of rat.

Methods and Results Randomly selected male Wistar rats were received ethanol (4.5 g⁄kg of 20% w⁄ v solution in saline) once per day for 6 week. Foam cell formation, blood pressure, and levels of intercellular adhesion molecule-1, vascular cell adhesion molecule-1, endothelial-leukocyte adhesion molecule-1, and high-sensitivity C-reactive protein (CRP) in ethanol treated rats were compared with sham and control rats. The results revealed a concurrent significant increase of adhesion molecules and CRP levels with significant increase of systolic, diastolic, pulse, and dicrotic pressure and formation of foam cell in ethanol-treated rats.

Conclusion these findings demonstrate that long-term ethanol consumption enables pro-atherogenic changes and stiffness in rat aorta wall via significant induction of proinflammatory response, augmenting of cell adhesion molecules and predisposition of endothelial dysfunction.

Key words: atherosclerosis; ethanol; endothelial dysfunction; cell adhesion molecules