Fira-Mladinescu O, Noveanu Lavinia, Ordodi V, Fira-Mladinescu Corneluţa, Tudorache V, Mihalaş Georgeta
Universitatea de Medicină şi Farmacie V. Babeş Timişoara, Facultatea de Medicină, Centrul de Studii în Medicina Preventivă.
Rev Med Chir Soc Med Nat Iasi. 2008 Jan-Mar;112(1):213-9.
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.
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.
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).
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.
长期让豚鼠暴露于香烟烟雾中会导致肺小动脉肌化，而内皮功能障碍可能是这种血管重塑的早期触发因素。因此，本研究旨在评估12周被动吸烟暴露对肺内皮血管舒缩功能的影响。
比较在器官浴中分离的、用去氧肾上腺素预收缩的肺动脉环，在累积剂量（10⁻⁹至10⁻⁴M）的内皮依赖性（乙酰胆碱、ACh和二磷酸腺苷、ADP）和非依赖性血管舒张剂（硝普钠、SNP）存在下的血管舒张反应。
我们的结果表明，长期让豚鼠暴露于香烟烟雾中仅会导致一氧化氮介导的内皮反应受损（10⁻⁵M乙酰胆碱时血管舒张为9.83±4.36%，而对照组为39.72±16.61%，p = 0.005；10⁻⁵M二磷酸腺苷时分别为36.64±7.21%，而对照组为55.53±13.51%，p = 0.02）。
对长期暴露于香烟烟雾中的豚鼠肺动脉血管舒缩功能进行体外研究，可能是评估慢性阻塞性肺疾病早期肺内皮功能障碍的可靠且相关的实验模型。
