Small Airway Pathology is Related to Increased Closing Capacity and Abnormal Slope of Phase III in Excised Human Lungs1–3

Publisher Website
Google Scholar
Abstract
Single-breath nitrogen and static pressure-volume curves were obtained from 29 excised human lungs. The lungs were separated into 2 groups based on values predicted for closing capacity; “normal” lungs (n = 19) had normal closing capacities, and “abnormal” lungs (n = 10) had closing capacities that were larger than normal. Closing pressure (the pressure at the onset of closing capacity) differed between the 2 groups. The group of abnormal lungs had a higher mean closing pressure (2.25 cm H2O) than that of the group of normal lungs (0.98 cm H2O) (p < 0.01). A grading system was used to estimate the extent of pathologic changes in the small airways of each whole lung. Mural inflammation and squamous metaplasia were 2 lesions of the small airways that differed significantly in degree (p < 0.05) between the 2 groups. Data from both groups were combined to determine whether any of the pathologic variables examined were correlated with the data from the single-breath nitrogen curves. Among the small airway lesions evaluated, only the degree of inflammatory cell infiltration (p < 0.01; r = 0.569) and increase in small airway smooth muscle (p < 0.05; r = 0.379) were significantly related to increased closing capacity. Occlusion of airways by luminal cells and mucus, mural inflammation, and increased airway muscle were all correlated with an increase in the slope of phase III, or alveolar plateau, expressed as a percentage of the predicted value, (p < 0.03). A good correlation was also found between closing pressure and closing capacity expressed as a percentage of the predicted value (p < 0.001; r = 0.68). We conclude that in excised human lungs, abnormal increases in closing capacity and slope of phase III are associated with increased closing pressure and pathologic changes in small airways.