Acute effects of cigarette smoke on Endothelial Nitric Oxide synthase, vascular cell adhesion molecule 1 and aortic intima media thickness

Abstract

Background. 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. 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). Methods. An experimental study with a post-test only controlled group design was used. We used 18 Wistar rats (Rattus norvegicus) 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. Results. 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 (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). Conclusion. Low e-NOS level and high VCAM-1 level observed after cigarette smoke exposure which may increase aortic IMT.

Preventive effect of Nigella sativa on M1/M2 ratio, reducing risk of endothelial dysfunction in cigarette smoked Wistars

“…24 A previous report by Ardiana et al showed that exposure to cigarette smoke decrease e-NOS level in the aorta. 25 A decline in e-NOS concentration led to not only increase in expression of adhesion molecules and vascular tone but also initiate inflammation coagulation cascade. 26 As a result, aortic intima-medial is thickening in the early step of atherosclerosis.…”

“…Excessive proliferation and apoptosis as compensation mechanism are responsible for vascular intimal media thickening. 25 Ardiana et al found not only an increase of intima-media thickness (IMT) but also structural changes marked by disorganization and vacuolization of smooth muscle cells in the tunica media of the aortic tissue. In addition, increased inflammatory process on the vascular endothelium are closely linked to atherosclerotic process.…”

Status Merokok Mempengaruhi Molekul Adhesi Sel Vaskular-1 Pada Perokok Pria Dengan Penyakit Kardiovaskular

“…Paparan asap rokok kronis dapat menyebabkan disfungsi endotel dengan meningkatkan ekspresi VCAM-1. 19 Beberapa bukti menyatakan bahwa perubahan endotel vaskular dimulai dengan pengurangan bioavailabilitas nitrit oksida (NO). Penurunan aktivitas NO akibat reaksi NO dari radikal bebas asap rokok dan kerusakan endotel dapat menyebabkan disfungsi endotel seperti vasodilatasi, antitrombotik, antiinflamasi dan antioksidan.…”

“…12 Sebuah Studi dari Meity et al menyatakan bahwa tingkat VCAM-1 meningkat pada tikus Wistar setelah 28 hari paparan asap rokok (40 batang per hari). 19 Perlu dicatat bahwa penelitian ini memiliki sejumlah keterbatasan. Pertama, data kami hanya berdasarkan catatan medis tanpa ada wawancara dengan pasien.…”