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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