Högman M, Frostell C G, Hedenström H, Hedenstierna G
Department of Clinical Physiology, University Hospital, Uppsala, Sweden.
Am Rev Respir Dis. 1993 Dec;148(6 Pt 1):1474-8. doi: 10.1164/ajrccm/148.6_Pt_1.1474.
We studied whether nitric oxide (NO), added at 80 ppm to inspired gas, can exert a bronchodilatory effect in humans. Four groups were studied: (1) healthy adult volunteers (n = 6), (2) adult subjects with hyperreactive airways (n = 6) during provocation with inhaled methacholine (MCh), (3) patients with bronchial asthma (n = 13), and (4) patients with chronic obstructive pulmonary disease (COPD, n = 6). All subjects were studied in a body plethysmograph, measuring volume-corrected specific airway conductance (SGaw). No patient or volunteer reacted with bronchoconstriction during NO inhalation. Nitric oxide did not affect SGaw in healthy volunteers or in patients with COPD. Inhaled NO modulated the MCh-induced bronchoconstriction toward dilatation. In patients with bronchial asthma, SGaw increased (p < 0.05) from 0.4 +/- 0.1 to 0.6 +/- 0.2 (kPa.s)-1. In a succeeding test with inhalation of a beta 2-agonist immediately after NO inhalation, a more marked increase in SGaw was seen, to 1.2 +/- 0.3 (kPa.s)-1 (p < 0.001). We conclude that NO inhaled at 80 ppm has no effect on airway tone in healthy volunteers, but modulates the response to MCh provocation toward bronchodilation. It exerts a weak bronchodilatory effect in bronchial asthma, but not in COPD.
我们研究了向吸入气体中添加80 ppm一氧化氮（NO）是否能对人体产生支气管舒张作用。研究了四组对象：（1）健康成年志愿者（n = 6），（2）吸入乙酰甲胆碱（MCh）激发试验期间气道反应性增高的成年受试者（n = 6），（3）支气管哮喘患者（n = 13），以及（4）慢性阻塞性肺疾病（COPD）患者（n = 6）。所有受试者均在体容积描记仪中进行研究，测量经容积校正的比气道传导率（SGaw）。在吸入NO期间，没有患者或志愿者出现支气管收缩反应。一氧化氮对健康志愿者或COPD患者的SGaw没有影响。吸入的NO将MCh诱导的支气管收缩调节为扩张。在支气管哮喘患者中，SGaw从0.4±0.1增加到0.6±0.2（kPa·s）-1（p < 0.05）。在吸入NO后立即吸入β2激动剂的后续试验中，SGaw出现更明显的增加，达到1.2±0.3（kPa·s）-1（p < 0.001）。我们得出结论，吸入80 ppm的NO对健康志愿者的气道张力没有影响，但可将对MCh激发试验的反应调节为支气管扩张。它在支气管哮喘中发挥微弱的支气管舒张作用，但在COPD中则不然。
