Effects of cigarette smoke on endothelial function of pulmonary arteries in the guinea pig.
Effects of cigarette smoke on endothelial function of pulmonary arteries in the guinea pig.
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DOI：
10.1186/1465-9921-10-76
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发表时间：
2009-08-14
影响因子：
5.8
通讯作者：
Barberà JA
中科院分区：
文献类型：
--
作者：
Ferrer E;Peinado VI;Díez M;Carrasco JL;Musri MM;Martínez A;Rodríguez-Roisin R;Barberà JA
吸烟可能会改变疾病早期阶段肺血管的结构和功能，从而导致慢性阻塞性肺疾病的肺动脉高压。本研究的目的是评估长期接触香烟烟雾对豚鼠肺动脉内皮功能和平滑肌细胞增殖的影响。 19 只雄性哈特利豚鼠每天暴露在 7 支香烟、每周 5 天的烟雾中，持续 3 个月和 6 个月。 17 只对照豚鼠在同一时期进行假暴露。通过 ADP 诱导的舒张来评估肺动脉和主动脉环的内皮功能。通过α-肌动蛋白和结蛋白的免疫组织化学表达评估肺小血管中平滑肌细胞的增殖及其表型。通过形态测量评估血管壁厚度、小动脉肌化和肺气肿。通过实时PCR评估内皮一氧化氮合酶(eNOS)的表达。暴露于香烟烟雾会减少肺动脉中内皮依赖性血管舒张（方差分析 p < 0.05），但不会减少主动脉中的内皮依赖性血管舒张。内皮功能障碍在暴露 3 个月时就很明显，并且在暴露 6 个月后没有进一步增加。暴露于烟雾的动物在暴露 3 个月后，小血管中分化不良的平滑肌细胞出现增殖 (p < 0.05)。长时间暴露导致小肺血管完全肌肉化（p < 0.05）、管壁增厚（p < 0.01）、主肺动脉收缩力增加（p < 0.05）以及肺泡腔扩大。暴露于香烟烟雾的动物的肺部 eNOS 表达降低。在豚鼠中，接触香烟烟雾会导致肺动脉选择性内皮功能障碍、肺小血管平滑肌细胞增殖以及肺内 eNOS 表达减少。这些变化在接触 3 个月后出现，并且先于肺气肿的发展。
Cigarette smoking may contribute to pulmonary hypertension in chronic obstructive pulmonary disease by altering the structure and function of pulmonary vessels at early disease stages. The objectives of this study were to evaluate the effects of long-term exposure to cigarette smoke on endothelial function and smooth muscle-cell proliferation in pulmonary arteries of guinea pigs. 19 male Hartley guinea pigs were exposed to the smoke of 7 cigarettes/day, 5 days/week, for 3 and 6 months. 17 control guinea pigs were sham-exposed for the same periods. Endothelial function was evaluated in rings of pulmonary artery and aorta as the relaxation induced by ADP. The proliferation of smooth muscle cells and their phenotype in small pulmonary vessels were evaluated by immunohistochemical expression of α-actin and desmin. Vessel wall thickness, arteriolar muscularization and emphysema were assessed morphometrically. The expression of endothelial nitric oxide synthase (eNOS) was evaluated by Real Time-PCR. Exposure to cigarette smoke reduced endothelium-dependent vasodilatation in pulmonary arteries (ANOVA p < 0.05) but not in the aorta. Endothelial dysfunction was apparent at 3 months of exposure and did not increase further after 6 months of exposure. Smoke-exposed animals showed proliferation of poorly differentiated smooth muscle cells in small vessels (p < 0.05) after 3 months of exposure. Prolonged exposure resulted in full muscularization of small pulmonary vessels (p < 0.05), wall thickening (p < 0.01) and increased contractility of the main pulmonary artery (p < 0.05), and enlargement of the alveolar spaces. Lung expression of eNOS was decreased in animals exposed to cigarette smoke. In the guinea pig, exposure to cigarette smoke induces selective endothelial dysfunction in pulmonary arteries, smooth muscle cell proliferation in small pulmonary vessels and reduced lung expression of eNOS. These changes appear after 3 months of exposure and precede the development of pulmonary emphysema.
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DOI：
10.1152/ajpheart.00029.2003
发表时间：
2003-09-01
影响因子：
4.8
作者：
Chatrath, R;Ronningen, KL;Miller, VM
通讯作者：
Miller, VM
影响因子：
--
作者：
JIN, NJ;PACKER, CS;RHOADES, RA
通讯作者：
RHOADES, RA
影响因子：
20.1
作者：
JOHNS, RA;LINDEN, JM;PEACH, MJ
通讯作者：
PEACH, MJ
影响因子：
9.6
作者：
Wright, JL;Churg, A
通讯作者：
Churg, A
影响因子：
15.9
作者：
Tschudi, MR;Barton, M;Luscher, TF
通讯作者：
Luscher, TF