UNLABELLED: Chronic exposure to cigarette smoke on guinea-pigs induced a muscularization of pulmonary arterioles and endothelial dysfunction might be an early trigger of this vascular remodelling. Accordingly, the present study was aimed to evaluate the effect of a 12 weeks exposure to passive smoking on the pulmonary endothelial vasomotor function. MATERIAL AND METHOD: Vasodilator response of pulmonary arteries rings isolated in organ bath, precontracted with phenylephrine, was compared in the presence of cumulative doses (10(-9) to 10(-4) M) of endothelial-dependent (acetylcholine, ACh and adenosine-diphosphate, ADP) and independent vasodilators (sodium nitroprusside, SNP), respectively. RESULTS: Our results suggest that chronic exposure of guinea-pigs to cigarette smoke induces the impairment only of NO-mediated endothelial response (vasodilation was 9.83 +/- 4.36 % for ACh 10(-5)M vs. 39.72 +/- 16.61 % in control, p = 0.005, respectively 36.64 +/- 7.21 % for ADP 10(-5)M vs. 55.53 +/- 13.51 %, p = 0.02). CONCLUSION: The in vitro study of pulmonary arteries vasomotor function in guinea pigs chronically exposed to cigarette smoke may represent a reliable and relevant experimental model for the assessment of pulmonary endothelial dysfunction in early stages of COPD.
UNLABELLED: Chronic exposure to cigarette smoke on guinea-pigs induced a muscularization of pulmonary arterioles and endothelial dysfunction might be an early trigger of this vascular remodelling. Accordingly, the present study was aimed to evaluate the effect of a 12 weeks exposure to passive smoking on the pulmonary endothelial vasomotor function. MATERIAL AND METHOD: Vasodilator response of pulmonary arteries rings isolated in organ bath, precontracted with phenylephrine, was compared in the presence of cumulative doses (10(-9) to 10(-4) M) of endothelial-dependent (acetylcholine, ACh and adenosine-diphosphate, ADP) and independent vasodilators (sodium nitroprusside, SNP), respectively. RESULTS: Our results suggest that chronic exposure of guinea-pigs to cigarette smoke induces the impairment only of NO-mediated endothelial response (vasodilation was 9.83 +/- 4.36 % for ACh 10(-5)M vs. 39.72 +/- 16.61 % in control, p = 0.005, respectively 36.64 +/- 7.21 % for ADP 10(-5)M vs. 55.53 +/- 13.51 %, p = 0.02). CONCLUSION: The in vitro study of pulmonary arteries vasomotor function in guinea pigs chronically exposed to cigarette smoke may represent a reliable and relevant experimental model for the assessment of pulmonary endothelial dysfunction in early stages of COPD.
Authors: Mohammad Hashemi; Mohammad Reza Afshani; Marjan Mansourian; Parinaz Poursafa; Roya Kelishadi Journal: J Res Med Sci Date: 2012-04 Impact factor: 1.852