Exposure to nitrogen dioxide is not associated with vascular dysfunction in man
Exposure to nitrogen dioxide is not associated with vascular dysfunction in man
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DOI：
10.3109/08958370903144105
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发表时间：
2010-02-01
影响因子：
2.1
通讯作者：
Blomberg, Anders
中科院分区：
文献类型：
--
作者：
Langrish, Jeremy P.;Lundback, Magnus;Blomberg, Anders
目的：为探讨二氧化氮暴露对血管收缩功能和纤溶功能的影响，采用随机双盲交叉研究方法，将10名健康男性志愿者在间歇性运动中暴露于4ppm的二氧化氮或过滤空气中1h。暴露后4小时，在单侧肱动脉内输注缓激肽（100-1000 pmol/min）、乙酰胆碱（5-20 μ g/min）、硝普钠（2-8 μ g/min）和维拉帕米（10-100 μ g/min）之前和期间测量双侧前臂血流和纤溶标志物。肺功能测定之前和之后的曝光，呼出一氧化氮在基线和1和4 h后exposed.Results：有没有在休息前臂血流量后，无论是曝光的差异。所有血管扩张剂均能使前臂血流量呈剂量依赖性增加，但两种血管扩张剂暴露后均相似（所有药物p > 0.05）。缓激肽引起血浆组织纤溶酶原激活剂的剂量依赖性增加，但同样没有差异的曝光。有肺功能或呼出的一氧化氮没有变化，无论是exposed.Conclusion：吸入二氧化氮不损害血管的血管或纤溶功能。二氧化氮似乎不是空气污染对心血管不利影响的主要仲裁者。
Objectives: To investigate the effect of nitrogen dioxide exposure on vascular vasomotor and six fibrinolytic functions.Methods: Ten healthy male volunteers were exposed to nitrogen dioxide at 4 ppm or filtered air for 1 h during intermittent exercise in a randomized double-blind crossover study. Bilateral forearm blood flow and fibrinolytic markers were measured before and during unilateral intrabrachial infusion of bradykinin (100-1000 pmol/min), acetylcholine (5-20 mu g/min), sodium nitroprusside (2-8 mu g/min), and verapamil (10-100 mu g/min) 4 h after the exposure. Lung function was determined before and after the exposure, and exhaled nitric oxide at baseline and 1 and 4 h after the exposure.Results: There were no differences in resting forearm blood flow after either exposure. There was a dose-dependent increase in forearm blood flow with all vasodilators but this was similar after either exposure for all vasodilators (p > .05 for all). Bradykinin caused a dose-dependent increase in plasma tissue-plasminogen activator, but again there was no difference between the exposures. There were no changes in lung function or exhaled nitric oxide following either exposure.Conclusion: Inhalation of nitrogen dioxide does not impair vascular vasomotor or fibrinolytic function. Nitrogen dioxide does not appear to be a major arbiter of the adverse cardiovascular effects of air pollution.