Airway nitric oxide output is reduced in bronchiectasis

• Published in: Respiratory medicine 2007-07, Vol.101 (7), p.1549-1555
• Main Authors: Foley, Susan C, Hopkins, Natalie O, Fitzgerald, Muiris X, Donnelly, Seamas C, McLoughlin, Paul
• Format: Article
• Language: English
• Subjects: Adult; Androstadienes - therapeutic use; Asthma; Biological and medical sciences; Breath Tests - methods; Bronchiectasis; Bronchiectasis - drug therapy; Bronchiectasis - metabolism; Bronchiectasis - physiopathology; Bronchodilator Agents - therapeutic use; Female; Fluticasone; Forced Expiratory Volume - drug effects; Glucocorticoid; Glucocorticoids - therapeutic use; Humans; Inducible nitric oxide synthase; Lungs; Male; Medical sciences; Middle Aged; Nitric oxide; Nitric Oxide - biosynthesis; Nitric Oxide - metabolism; Nitric Oxide Synthase Type II - metabolism; Pneumology; Pulmonary Alveoli - metabolism; Pulmonary/Respiratory; Respiratory system : syndromes and miscellaneous diseases; Rodents; Vital Capacity - drug effects
• ISSN: 0954-6111; 1532-3064
• DOI: 10.1016/j.rmed.2006.12.005

Summary Background Increased concentrations of exhaled nitric oxide (NO) have been detected in inflammatory lung diseases including asthma and have been attributed to increased expression and activity of inducible nitric oxide synthase (iNOS) within the airways. However, previous studies of exhaled NO in patients with bronchiectasis have yielded conflicting results, with reports of both increased and normal NO values. Recent evidence from animal models suggests that chronic airway infection reduces NO production within the lung, despite causing increased iNOS expression. We tested the hypothesis that, in human subjects with bronchiectasis, chronic airway infection reduces NO output from the conducting airways. Methods Using a recently described two-compartment model, we measured separately the contributions of the conducting airways and the alveoli to exhaled NO in nine patients with stable bronchiectasis and eight control subjects before and after inhaled glucocorticoid therapy. Results We found that airway NO output was significantly lower in bronchiectasis than in normal airways whereas NO output from the alveoli was similar to that of control subjects. High-dose inhaled glucocorticoid therapy did not alter airway or alveolar NO production. Conclusions These findings demonstrate that, in patients with bronchiectasis, airway NO output is reduced and that iNOS does not contribute significantly to airway NO production.