title: Inhaled fluticasone decreases bronchial but not alveolar nitric oxide output in asthma.
abstract: Exhaled nitric oxide (NO) concentration is a noninvasive measure of airway inflammation and is increased in asthma. Inhaled glucocorticoids decrease exhaled NO concentration, but the relative contributions of alveolar and bronchial levels to the decrease in exhaled NO concentration are unknown. Alveolar NO concentration and bronchial NO flux can be separately approximated by measuring exhaled NO at several exhalation flow rates. The effect of steroid treatment on alveolar and bronchial NO output in asthma was studied. Alveolar NO concentration and bronchial NO flux were assessed in 16 patients with asthma before and during treatment with inhaled fluticasone for 8 weeks and in 16 healthy controls. Before the treatment, asthmatics had increased bronchial NO flux (mean+/-SEM: 3.6+/-0.4 versus 0.7+/-0.1 nL x s(-1), p<0.001) but normal alveolar NO concentration (1.2+/-0.5 versus 1.0+/-0.2 parts per billion (ppb), p>0.05) compared with controls. Inhaled fluticasone decreased bronchial NO flux from 3.6+/-0.4 to 0.7+/-0.1 nL x s(-1) (p<0.01) but had no effect on alveolar NO concentration (before: 1.2+/-0.5; after: 1.2+/-0.1 ppb, p>0.05). The forced expiratory volume in one second improved, whereas asthma symptom score and serum levels of eosinophil cationic protein and eosinophil protein X decreased during the treatment. In conclusion, inhaled fluticasone decreases bronchial but not alveolar nitric oxide output simultaneously with clinical improvement in patients with asthma.
authors.affiliation: The Immunopharmacological Research Group, Medical School, University of Tampere, Dept of Clinical Chemistry, Finland.
authors.forename: L
authors.initials: L
authors.lastname: Lehtimäki
authors.forename: H
authors.initials: H
authors.lastname: Kankaanranta
authors.forename: S
authors.initials: S
authors.lastname: Saarelainen
authors.forename: V
authors.initials: V
authors.lastname: Turjanmaa
authors.forename: E
authors.initials: E
authors.lastname: Moilanen
mesh_terms: D000280:Administration, Inhalation; D000328:Adult; D000730:Androstadienes / Q000008:administration & dosage*; D018927:Anti-Asthmatic Agents / Q000008:administration & dosage*; D000893:Anti-Inflammatory Agents / Q000008:administration & dosage*; D001249:Asthma / Q000188:drug therapy / Q000378:metabolism* / Q000503:physiopathology; D001798:Blood Proteins / Q000032:analysis; D001944:Breath Tests; D001980:Bronchi / Q000378:metabolism*; D047091:Eosinophil Granule Proteins; D047208:Eosinophil-Derived Neurotoxin; D005260:Female; D000068298:Fluticasone; D005541:Forced Expiratory Volume; D006801:Humans; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism*; D011650:Pulmonary Alveoli / Q000378:metabolism*; D012260:Ribonucleases / Q000097:blood
chemical_list: D000730:Androstadienes; D018927:Anti-Asthmatic Agents; D000893:Anti-Inflammatory Agents; D001798:Blood Proteins; D047091:Eosinophil Granule Proteins; D018836:Inflammation Mediators; D009569:Nitric Oxide; D000068298:Fluticasone; D047208:Eosinophil-Derived Neurotoxin; D012260:Ribonucleases