Relaxation of human peripheral airway smooth muscle in vitro does not correlate with severity of chronic airflow limitation in vivo.

We tested the hypothesis that a defect in relaxation of peripheral airway smooth muscle contributes to chronic airflow limitation in chronic obstructive pulmonary disease (COPD). Twenty subjects underwent lung function measurements prior to thoracotomy. Lung tissue was obtained during surgery and bronchiolar segments were dissected. Smooth muscle function was measured isotonically in organ baths, using L-isoprenaline and the adenylate cyclase activator forskolin. Segments were precontracted with methacholine. Of the 20 subjects, 10 fulfilled the ATS criteria for COPD and had airflow limitation. There was no significant relationship between the degree of airflow limitation in vivo and the sensitivity or maximal response of peripheral airway muscle to methacholine, L-isoprenaline or forskolin in vitro. Furthermore, we found no differences between the mean contractile- and relaxation responses of airways from subjects with versus those without COPD and airflow limitation. Lung tissue from patients who regularly used beta-adrenergic drugs (n = 3) and/or steroids (n = 3) exhibited responses in vitro similar to those from subjects without medication. These results suggest that airflow limitation in COPD is not associated with an impaired relaxability of peripheral airway smooth muscle.