Hazucha M J, Ginsberg J F, McDonnell W F, Haak E D, Pimmel R L, Salaam S A, House D E, Bromberg P A
J Appl Physiol Respir Environ Exerc Physiol. 1983 Mar;54(3):730-9. doi: 10.1152/jappl.1983.54.3.730.
It has been reported (J. Clin. Invest. 57: 301-307, 1976) that inhalation of nitrogen dioxide (NO2) will enhance the bronchial reactivity of asthmatics. This study was designed to evaluate the respiratory effect of a 1-h exposure of normal subjects and of atopic asthmatics to 0.1 parts per million (ppm) NO2. Fifteen normal and 15 asthmatic subjects were exposed to air and to NO2 in a randomized double-blind crossover design. Exposure to either atmosphere was bracketed by bronchial inhalation challenge using aerosolized metacholine chloride solutions. Plethysmographic measurements of specific airway resistance (sRaw) and the forced random noise impedance spectrum (5-30 Hz) were obtained immediately after each methacholine dose. Following acute exposure to NO2, there was a slight but not significant increase in mean base-line sRaw in both normals and asthmatics. The overall base-line resistive properties of the respiratory system determined by forced random noise excitation were not significantly affected by NO2 inhalation either. Finally, there was no change in bronchial response to methacholine challenge in either group. These findings indicate that 0.1 ppm NO2 exposure for 1 h without exercise had no demonstrable airways effects in either young atopic asthmatics with mild disease or young normal subjects.
据报道(《临床研究杂志》57: 301 - 307, 1976),吸入二氧化氮(NO₂)会增强哮喘患者的支气管反应性。本研究旨在评估正常受试者和特应性哮喘患者暴露于百万分之一(ppm)的NO₂ 1小时后的呼吸效应。15名正常受试者和15名哮喘患者按照随机双盲交叉设计暴露于空气和NO₂环境中。每次暴露于任何一种环境前后,均通过雾化氯化乙酰甲胆碱溶液进行支气管吸入激发试验。每次给予乙酰甲胆碱后,立即通过体积描记法测量比气道阻力(sRaw)和强迫随机噪声阻抗谱(5 - 30 Hz)。急性暴露于NO₂后,正常受试者和哮喘患者的平均基线sRaw均有轻微但不显著的增加。通过强迫随机噪声激发测定的呼吸系统总体基线阻力特性也未受到NO₂吸入的显著影响。最后,两组对乙酰甲胆碱激发试验的支气管反应均无变化。这些发现表明,在无运动情况下,暴露于0.1 ppm的NO₂ 1小时对患有轻度疾病的年轻特应性哮喘患者或年轻正常受试者均未产生明显的气道影响。