Acute Effects of Cigarette on Endothelial Nitric Oxide Synthase, Vascular Cell Adhesion Molecule 1 and Aortic Intima Media Thickness “Cigarette smoke–induced pro-atherogenic changes”

Abstract

BackgroundCigarette smoking could induce endothelial dysfunction and increase of circulating markers of inflammation by activation of monocytes. This can lead to the increased of intima media thickness (IMT) of entire blood vessel and result acceleration of atherosclerosis process. However, to our knowledge, little is known about the role of cigarette smoking in this atherosclerotic inflammatory process.ObjectiveThe aim of this study is to explore the link between cigarette smoking on endothelial nitric oxide synthase (e-NOS) and vascular cell adhesion molecule 1 (VCAM-1).MethodsAn experimental study with post-test only controlled group design was used in this study. We used 18 Wistar rats (Rattus norvegicus) randomly subdivided into 2 groups, group K (−) were given no tobacco smoking exposed, whereas group K (+) were exposed to 40 cigarettes smokes daily. After 28 days, samples were analyzed for e-NOS, VCAM-1 and aortic IMT.ResultsOur results indicate that tobacco smoke can enhance the expression of VCAM-1 on mouse cardiac vascular endothelial cell, resulting in decreased expression of e-NOS level and increased of aortic IMT. Linear regression model found that eNOS level negatively correlated wiith aortic IMT (r2 = 0.584, β = −0.764, p < 0.001), whereas VCAM-1 expression did not correlate with aortic IMT (r2 = 0.197, p = 0.065).ConclusionLow e-NOS level and high VCAM-1 level observed following after cigarette smoke exposure may increase aortic IMT.Clinical significanceIncreasing evidence suggests that cigarette smoke exposure could induce VCAM-1 (enhance pro-atherogenic property),and decreased of e-NOS level (anti-atherogenic depletion). Thus, cigarette smoke may represent a significant risk factor for atherosclerosis by increasing aortic IMT. This evidence is discussed herein.