Sanna A, Kurtansky A, Veriter C, Stănescu D
Pulmonary Laboratory and Division, Cliniques Universitaires Saint Luc, Brussels, Belgium.
Am J Respir Crit Care Med. 1994 Dec;150(6 Pt 1):1702-4. doi: 10.1164/ajrccm.150.6.7952636.
Studies in animals have shown that inhalation of nitric oxide (NO) either reduced pulmonary resistance after an induced bronchospasm or protected animals from bronchoconstriction. To evaluate whether NO inhalation (80 parts per million) influences basal bronchial tone or reverses methacholine-induced bronchospasm, we determined specific airway conductance (SGaw) as a measure of airway caliber in seven healthy men. After methacholine-induced bronchoconstriction NO increased SGaw by 23% (p < 0.05). One week later, NO inhalation did not change baseline SGaw values. However, albuterol inhaled after NO, or on a separate day, significantly increased SGaw (p < 0.05). The bronchodilator effect of NO in men with methacholine-induced bronchospasm is much less than that reported in animals or that regularly observed in asthmatic patients after the inhalation of beta-sympathomimetic drugs.
动物研究表明，吸入一氧化氮（NO）可降低诱发支气管痉挛后的肺阻力，或保护动物免受支气管收缩影响。为评估吸入NO（百万分之80）是否会影响基础支气管张力或逆转乙酰甲胆碱诱发的支气管痉挛，我们测定了7名健康男性的比气道传导率（SGaw），以此作为气道管径的指标。在乙酰甲胆碱诱发支气管痉挛后，NO使SGaw增加了23%（p < 0.05）。一周后，吸入NO并未改变基线SGaw值。然而，在吸入NO后或在另一天吸入沙丁胺醇，可显著增加SGaw（p < 0.05）。在患有乙酰甲胆碱诱发支气管痉挛的男性中，NO的支气管扩张作用远小于动物研究中报道的作用，也远小于哮喘患者吸入β-拟交感神经药物后通常观察到的作用。
