Cigarette Smoke Extract Impairs Endothelium-Dependent Relaxation in Isolated Rat Aortic Rings
Ovidiu Fira-Mladinescu1, Dan M. Danila2, Mircea Hancu1, Corneluţa Fira-Mladinescu3, Danina Muntean1, Smaranda R. Goţia4, and Alexandru Cristescu1
1Departments of Pathophysiology, 2Biochemistry, 3Hygiene, and 4Physiology, Victor Babeş Unversity of Medicine and Pharmacy, Timişoara, Romania
Corresponding author: Ovidiu Fira-Mladinescu
Department of Pathophysiology
Victor Babeş University of Medicine and Pharmacy
Str. Eftimie Murgu no. 2
RO-300041, Timişoara, Romania
Telephone: +40-256-220479
Fax number: +40-256-220479
E-mail: mladinescu@umft.ro
CEJOEM 2004, Vol.10. No.1.: 18–24
Key words:
Cigarette smoking, endothelial dysfunction, rat aortic ring
Abstract:
While clear-cut epidemiological, morphological, and functional proofs are available to
substantiate that cigarette smoking is deleterious to the vascular endothelium, there are no
conclusive previous experiments with regard to its effect on endothelium-dependent vasodilation.
The aim of this study was to examine the effects of the water soluble component of cigarette
smoke extract (CSE) on endothelium-dependent and endothelium-independent vasodilation in the
isolated aortic rings of rats. In this preparation, preincubation with CSE attenuated the
acetylcholine-mediated endothelium-dependent relaxation while the endothelium-independent one
induced by sodium nitroprusside did not change. Our results indicate that cigarette smoke may
induce primary endothelial dysfunction by decreasing the release of endothelium-derived relaxing
factor (NO) in the vascular endothelial cells and/or its activity in the vascular smooth muscle
cells. The rat’s isolated aortic ring provides a reliable and reproducible experimental model
that can be used for in vitro investigation of the mechanisms involved in cigarette
smoking-induced endothelial dysfunction.
Received: 1 August 2003
Accepted: 23 February 2004
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