Smoking is a risk factor for the development of atherosclerosis. However, the exact mechanism of smoking-related damage to the arterial wall and its relation to the atherosclerotic process are not known. The endothelium plays an important role for the regulation of vascular tone and its function is impaired in the presence of risk factors early in the process of atherosclerosis. To assess the effect of smoking on endothelium-dependent relaxation, we examined vascular reactivity in vitro in an animal model of environmental tobacco smoke exposure.

Guinea pigs were randomized to control group or environme-ntal tobacco smoke exposure group. The source of environmental tobacco smoke exposure was sidestream smoke during 6 hours per day and 5 days per week over 6 weeks or 12 weeks in a smoking chamber. Fresh aortic rings were suspended in organ baths (37℃, 95%O2-5%CO2). Rings were precontracted with phenylephrine (10-7 M) and exposed to acetylcholine (10-7-10-4 M) and sodium nitroprusside (10-7-10-5 M) in increasing doses and isometric tension was recorded to evaluate the endothelium-dependent and -independent relaxation.

Acetylcholine-induced maximal relaxation (mean±SD) was 18±9% in the rings from the 6-week smoked guinea pigs and 4±3% in the rings from the 12-week smoked guinea pigs in comparison with 49±6% of the controls (p<0.05). The endothelium-dependent relaxation of the rings from 12 week-exposure was significantly less than that of 6 week-exposure. In contrast endothelium-independent relaxation to sodium nitroprusside was not different among three groups.

Environmental tobacco smoke exposure impairs endothelial function in guinea pig aorta.