Airway Distensibility in Adults with Asthma and Healthy Adults, Measured by Forced Oscillation Technique

Abstract

Reduced airway distensibility in subjects with asthma compared with control subjects may be related to differences in lung elastic recoil and bronchomotor tone. To examine the contribution of lung elastic recoil and bronchomotor tone to airway distensibility. We compared airway distensibility in 18 subjects with asthma with 19 control subjects before and after bronchodilator administration and, in a subgroup of 7 subjects with asthma and 8 control subjects, correlated distensibility with pressure-volume parameters. Distensibility was measured, using the forced oscillation technique, as the linear slope of conductance versus volume between total lung capacity (TLC) and 75% TLC and between 75% TLC and FRC. Transpulmonary pressure was recorded concurrently with distensibility, using an esophageal balloon. Pressure-conductance data were described using linear regressions and pressure-volume data were described using exponential equations. Subjects with asthma had lower baseline FEV1 (p=0.0003) and conductance (p=0.002) than did control subjects. Distensibility above 75% TLC was less in subjects with asthma than in control subjects (p<0.0001), but there was no difference below 75% TLC. Bronchodilator administration did not alter distensibility despite increases in FEV1 (p=0.0002) and conductance (p<0.0001) in subjects with asthma, and conductance (p=0.0004) in control subjects. After bronchodilator administration, subjects with asthma had reduced lung elastic recoil compared with control subjects (p=0.03) and a reduced pressure-conductance slope (p=0.01), but there were no correlations between pressure-volume characteristics and airway distensibility. Airway distensibility measured by forced oscillation technique is reduced in subjects with asthma compared with subjects without asthma, is not related to lung elastic recoil, and is unchanged by bronchodilator administration. Airway wall remodeling remains the most likely cause of reduced airway distensibility in asthma.