CIGARETTE-SMOKING INCREASES ENDOTHELIAL-DERIVED VASORELAXATION IN THERAT CAROTID-ARTERY IN A DOSE-DEPENDENT MANNER

Citation
S. Nene et al., CIGARETTE-SMOKING INCREASES ENDOTHELIAL-DERIVED VASORELAXATION IN THERAT CAROTID-ARTERY IN A DOSE-DEPENDENT MANNER, The Journal of surgical research, 71(2), 1997, pp. 101-106
Citations number
30
Categorie Soggetti
Surgery
ISSN journal
00224804
Volume
71
Issue
2
Year of publication
1997
Pages
101 - 106
Database
ISI
SICI code
0022-4804(1997)71:2<101:CIEVIT>2.0.ZU;2-4
Abstract
While there is clear-cut epidemiologic, morphologic, and functional ev idence to suggest that cigarette smoking is deleterious to the cardiov ascular system and endothelium, previous experiments with regard to th e effect of cigarette smoking on endothelial-derived vasorelaxation ar e not conclusive. This study examines the effect of cigarette smoking on endothelium-derived vasorelaxation and its relationship to serum ni tric oxide concentrations. Fourteen Sprague-Dawley rats (350-500 g) we re divided into two groups (N = 7). The experimental group was exposed to six cigarettes (Kentucky 1R4F) per day for 50 days casing a Griffi th snout exposure method. The two groups were sacrificed and the carot id arteries were mounted on isometric force transducers in a physiolog ic bath. The arteries were constricted with norepinephrine (1 x 10(-4) M). Vasorelaxation to acetylcholine (Ach) was measured in a dose resp onse manner. Vasorelaxation to nitroglycerin was measured at 10(-4) M. After the rats were sacrificed, blood samples from each rat were exam ined for total nitrate/nitrite concentration with serum chemiluminesce nce on a vanadium column. The results were analyzed with ANOVA and the Student's t test. Vasorelaxation to nitroglycerin was 17.42% +/- 0.44 versus 16.25% +/- 0.42 in the control and smoke exposure groups, resp ectively (P = 0.19). This experiment counterintuitively demonstrates t hat cigarette smoking augments endothelial-derived vasorelaxation. No effect was noted in the endothelium-independent vasorelaxation to nitr oglycerin. Alternative mechanisms including the presence of hypoxia an d exogenous nitric oxide, which lead to endothelial-dependent and -ind ependent vasorelaxation secondary to cigarette smoking, may serve to e xplain the apparent augmentation of endothelial-derived vasorelaxation . Further experiments with isolated components of smoke will need to b e done to resolve the debate. (C) 1997 Academic Press.