Background: An important role for exhaled nitric oxide (NO) measurement could be in the distinction between proximal and peripheral lung contributions to inflammation, with a particular interest for the alveolar lung zone and its implication on airway function.
Objective: We aimed to isolate the acinar lung zone contribution to both inflammation and airway function to seek a relationship between them.
Methods: In 30 patients with asthma with an asthma control test score exceeding 20, indices of conductive and acinar ventilation heterogeneity (Scond, Sacin) were obtained from a multiple breath washout. NO production in the conductive airways (J'aw(NO)), alveolar NO concentration (CA(NO)), and the standard exhaled NO at 50 mL/s (FENO(50)) were obtained from exhaled NO.
Results: Scond was consistently abnormal in all patients with stable asthma, but without any correlation to inflammation abnormality in that compartment (J'aw(NO)). Sacin was particularly abnormal in the asthma subgroup receiving >500 microg budesonide equivalent, and a correlation was found between Sacin and CA(NO) (r = 0.61; P = .015); in this subgroup, a weak association was found between Scond and J'aw(NO) or FENO(50) (r = 0.50; P = .059 for both).
Conclusion: The persistent functional abnormality of small conductive airways in patients with stable asthma is largely independent of inflammation as measured by exhaled NO. In the alveolar compartment, a functional correlate of alveolar NO was found in a subgroup of patients with stable asthma on moderate-to-high maintenance doses of inhaled steroids. These patients in particular could benefit from novel therapies specifically aimed at improving airway functionality at the level of the acinar entrance and beyond.