Key result
Cigarette smoke exposure for 28 days significantly increased aortic intima media thickness (88.39 μm vs 58.98 μm) and decreased endothelial nitric oxide synthase levels in male Wistar rats.
Why the study?
Little was known about the role of cigarette smoking in the atherosclerotic inflammatory process, prompting exploration of its effect on e-NOS and VCAM-1.
Does cigarette smoke exposure increase aortic IMT and alter e-NOS and VCAM-1 levels in Wistar rats?
Does cigarette smoke exposure increase aortic IMT and alter e-NOS and VCAM-1 levels in Wistar rats?
Absolute Event Rate: 88.39% vs 58.98%
p-value: p=<0.001
Cigarette smoke exposure decreases e-NOS levels and increases aortic IMT in a rat model, highlighting a potential mechanism for smoking-induced atherogenesis.
Supports smoking-induced endothelial changes in rats; leaves open human translation and clinical relevance.
<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. (2023) studied Endothelial dysfunction and atherosclerosis (n=18). Cigarette smoke vs. No tobacco smoke exposure was evaluated on Aortic Intima Media Thickness (IMT) in μm (p=<0.001). Cigarette smoke exposure for 28 days significantly increased aortic intima media thickness (88.39 μm vs 58.98 μm) and decreased endothelial nitric oxide synthase levels in male Wistar rats.
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