Key result
Exposure to cigarette smoke for 28 days significantly increased aortic intima media thickness to 88.39 μm compared to 58.98 μm in the unexposed control group of male Wistar rats.
Why the study?
Little is known about the role of cigarette smoking in the atherosclerotic inflammatory process leading to increased intima media thickness.
Does tobacco smoke exposure decrease e-NOS and increase VCAM-1 and aortic IMT in Wistar rats?
Does tobacco smoke exposure decrease e-NOS and increase VCAM-1 and aortic IMT in Wistar rats?
Absolute Event Rate: 88.39% vs 58.98%
p-value: p=<0.001
Cigarette smoke exposure acutely decreases e-NOS levels and increases aortic IMT in a rat model, highlighting a potential mechanism for smoking-induced atherogenesis.
Hypothesis-generating for smoke-related aortic remodeling in animals; leaves open translation to human cardiovascular risk.
<ns4:p> <ns4:bold>Background</ns4:bold> . Cigarette smoking could induce endothelial dysfunction and the increase of circulating markers of inflammation by activation of monocytes. This can lead to increased intima media thickness (IMT) of entire blood vessels and result in acceleration of the atherosclerosis process. However, to our knowledge, little is known about the role of cigarette smoking in this atherosclerotic inflammatory process. </ns4:p> <ns4:p>The aim of this study is to explore the link between cigarette smoking and its effect on endothelial nitric oxide synthase (e-NOS) and vascular cell adhesion molecule 1 (VCAM-1).</ns4:p> <ns4:p> <ns4:bold>Methods</ns4:bold> . An experimental study with a post-test only controlled group design was used. We used 18 Wistar rats ( <ns4:italic>Rattus norvegicus</ns4:italic> ) randomly subdivided into two groups: group K (-) were not exposed to tobacco smoke, whereas group K (+) were exposed to smoke equivalent of more than 40 cigarettes for 28 days daily. After 28 days, samples were analyzed for e-NOS, VCAM-1 and aortic IMT. </ns4:p> <ns4:p> <ns4:bold>Results</ns4:bold> <ns4:italic>.</ns4:italic> Our results indicate that tobacco smoke can enhance the expression of VCAM-1 on rat cardiac vascular endothelial cells, resulting in a decreased expression of e-NOS level and increase of aortic IMT. Linear regression model found that eNOS level negatively correlated wiith aortic IMT ( <ns4:italic>r</ns4:italic> <ns4:sup>2</ns4:sup> = 0.584, β = -0.764, <ns4:italic> <ns4:italic>p</ns4:italic> </ns4:italic> <ns4:bold> </ns4:bold> < 0.001), whereas VCAM-1 expression did not correlate with aortic IMT ( <ns4:italic>r</ns4:italic> <ns4:sup>2</ns4:sup> = 0.197, <ns4:italic> <ns4:italic>p</ns4:italic> </ns4:italic> <ns4:bold> </ns4:bold> = 0.065). </ns4:p> <ns4:p> <ns4:bold>Conclusion</ns4:bold> . Low e-NOS level and high VCAM-1 level observed after cigarette smoke exposure which may increase aortic IMT. </ns4:p>
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Ardiana et al. (2022) studied Endothelial dysfunction (n=18). Cigarette smoke vs. No tobacco smoke exposure was evaluated on Aortic intima media thickness (IMT) (p=<0.001). Exposure to cigarette smoke for 28 days significantly increased aortic intima media thickness to 88.39 μm compared to 58.98 μm in the unexposed control group of male Wistar rats.
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