Short-term passive smoking causes endothelial dysfunction via oxidative stress in nonsmokers
Short-term passive smoking causes endothelial dysfunction via oxidative stress in nonsmokers
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DOI：
10.1139/y06-030
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发表时间：
2006-05-01
影响因子：
2.1
通讯作者：
Node, Koichi
中科院分区：
文献类型：
--
作者：
Kato, Toru;Inoue, Teruo;Node, Koichi
最近的研究表明，被动吸烟损害血管内皮功能，并诱导人体氧化应激。然而，在大多数关于烟草诱导的病理生理学的先前人类数据中，血管内皮功能障碍和氧化应激已被单独评估。本研究旨在确定被动吸烟对血管内皮功能的急性影响与体内氧化应激状态之间的关系。我们研究了30名健康男性日本志愿者（32 +/- 7岁），包括15名习惯性吸烟者和15名非吸烟者。基线超声心动图，血流动力学记录和血液采样后，受试者暴露于被动吸烟30分钟。内皮依赖性血管舒张通过使用%流量介导的血管舒张（%FMD）的肱动脉和血浆水平的8-异前列腺素通过酶免疫测定法测量之前和之后的被动吸烟暴露。与非吸烟者相比，吸烟者的基线%FMD较低（4.3% +/- 1.2% vs. 10.9% +/-3.1%，p < 0.001），基线血浆8-异前列烷水平较高（41.5 +/- 5.8 pg/mL vs. 26.9 +/- 5.4 pg/mL，p < 0.001）。吸烟者被动吸烟后，%FMD和8-异前列烷水平没有变化。然而，在非吸烟者中，被动吸烟暴露30分钟后，%FMD降低（至5.0% +/-1.9%，p < 0.001），8-异前列烷水平显著升高（至37.8 +/- 9.6 pg/mL，p < 0.001），与吸烟者的水平相当。所有患者被动吸烟前后校正的60份样本中，% FMD与血浆8-异前列腺素水平呈显著负相关（n = 60，r =-0.69，p < 0.001）。即使是30分钟的被动吸烟也会迅速损害血管内皮功能，这与氧化应激有关。我们的数据提供了病理生理学的见解，最近的流行病学证据表明，冠心病的风险增加的非吸烟者暴露于被动吸烟。
Recent studies have shown that passive smoking impairs vascular endothelial function and induces oxidative stress in humans. However, in most of the previous human data regarding tobacco-induced pathophysiology, vascular endothelial dysfunction and oxidative stress have been separately assessed. This study was designed to determine the association between the acute effect of passive smoking on vascular endothelial function and in-vivo oxidative stress status. We studied 30 healthy male Japanese volunteers (32 +/- 7 years) including 15 habitual smokers and 15 nonsmokers. After baseline echocardiographic, hemodynamic recording, and blood sampling, subjects were exposed to passive smoking for 30 min. Endothelium-dependent vasodilation was measured by using % flow-mediated vasodilation (%FMD) of the brachial artery and plasma levels of 8-isoprostane was measured by enzyme immunoassay before and after the passive smoking exposure. Baseline %FMD was lower (4.3% +/- 1.2% vs. 10.9% +/- 3.1%, p < 0.001) and baseline plasma 8-isoprostane level was higher (41.5 +/- 5.8 pg/mL vs. 26.9 +/- 5.4 pg/mL, p < 0.001) in smokers than those in nonsmokers. The %FMD and 8-isoprostane level did not change after passive smoking in smokers. In nonsmokers, however, the %FMD decreased (to 5.0% +/- 1.9%, p < 0.001) and the 8-isoprostane level increased (to 37.8 +/- 9.6 pg/mL, p < 0.001) significantly after 30 min passive smoking exposure, equivalently to the levels of smokers. Sixty corrected samples before and after passive smoking exposure in all patients showed a significant negative correlation between the % FMD and the plasma 8-isoprostane levels (n = 60, r = -0.69, p < 0.001). Even 30 min of passive smoking rapidly impairs vascular endothelial function, which is associated with oxidative stress. Our data provide the pathophysiological insight for the recent epidemiological evidence about the increased risk of coronary heart disease among nonsmokers exposed to passive smoking.