Cigarette smoke extract induces endothelium dysfunction in isolated rabbit pulmonary arteries via an oxidative mechanism

In early stages of COPD, lacking hypoxemia, pulmonary arteries yet show endothelial abnormalities. This vascular impairment could be assigned to noxious effects of some cigarette smoke components. The aim of the present study was to investigate the effect of cigarette smoke extract (CSE) on endothelial vasomotor function in isolated rabbit pulmonary arteries in the presence or absence of a natural antioxidant with superoxide dismutase activity (SODn). After incubation of vascular rings with CSE (5% in organ bath) vascular responses to acetylcholine (endothelial-dependent vasodilator agent) and sodium nitroprusside (endothelial-independent vasodilator agent) were evaluated. Our results showed the impairment of endothelial dependent vasodilation (maximal relaxation expressed as % was 28.32 +/- 10.15 vs. 46.36 +/- 8.04 in the group coincubated with SODn, p < 0.01) while endothelial independent relaxation was preserved (maximal response expressed as % was 95.04 +/- 7.40 vs. 97.54 +/- 4.58 in the group coincubated with natural antioxidant, p = NS). In conclusion, the hydrosoluble components of CSE induced endothelial vasomotor function impairment, most probable, via an oxidative mechanism.