RT期刊论文SR电子T1臭氧引起的肺部功能递减不相关早期呼吸道炎症或抗氧化剂应答JF欧洲呼吸杂志JO欧洲呼吸ĴFD欧洲呼吸协会SP 1418 OP 1428 VO 13 6 A1布贝格，A A1 Mudway，IS188bet官网地址A1 Nordenhall，C A1 Hedenstrom，H A1凯利，FJ A1弗鲁，AJ A1霍尔盖特，ST A1桑德斯特伦，T YR 1999年UL //www.qdcxjkg.com/content/13/6/1418.abstract AB这项研究试图澄清健康人类受试者进行适度的间歇性运动以下臭氧挑战的气道内发生的早期事件。十三健康不吸烟的受试者在单一盲暴露，交叉控制的方式为每百万（ppm）0.2份O3和使用一个标准的间歇运动与休息协议过滤的空气2小时，。肺功能评估前，并立即暴露后。支气管镜的曝光期间的结束后，用支气管粘膜活检，支气管洗涤（BW）和支气管肺泡灌洗（BAL）1.5小时进行。呼吸道衬液（RTLF）氧化还原状态，通过测量一定范围的抗氧化剂和在BW氧化损伤标记物和BAL流体样品的评估。有臭氧暴露于血管内皮P-选择（P <0.005）和细胞间粘附分子-1（P <0.005）的表达之后的显著上调。这是与在粘膜下肥大细胞活检样品中（P <0.005）的2倍的增加相关联，而不中性粒细胞炎症的证据，而在BAL液巨噬细胞数目的减少（1.6倍，P <0.005），与激活剩余的巨噬细胞子集（以％人类白细胞抗原（HLA）-DR +细胞，p <0.005 2.5倍的增加）。 In addition, exposure led to a 4.5-fold and 3.1-fold increase of reduced glutathione (GSH) concentrations, in BW and BAL fluid respectively (p<0.05), with alterations in urate and alpha-tocopherol plasma/RTLF partitioning ratios (p<0.05). Spirometry showed reductions in forced vital capacity (p<0.05) and forced expiratory volume in one second (p<0.01), with evidence of small airway narrowing using forced expiratory flow values (p<0.005). Evidence was found of O3-induced early adhesion molecule upregulation, increased submucosal mast cell numbers and alterations to the respiratory tract lining fluid redox status. No clear relationship was demonstrable between changes in these early markers and the lung function decrements observed. The results therefore indicate that the initial lung function decrements are not predictive of, or causally related to the O3-induced inflammatory events in normal human subjects.