RT Journal Article
SR Electronic
T1 Physiological and morphological determinants of maximal expiratory flow in chronic obstructive lung disease
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP 1785
OP 1794
DO 10.1183/09031936.96.09091785
VO 9
IS 9
A1 HA Tiddens
A1 JM Bogaard
A1 JC de Jongste
A1 WC Hop
A1 HO Coxson
A1 PD Pare
YR 1996
UL http://erj.ersjournals.com/content/9/9/1785.abstract
AB Maximal expiratory flow in chronic obstructive pulmonary disease (COPD) could be reduced by three different mechanisms; loss of lung elastic recoil, decreased airway conductance upstream of flow-limiting segments; and increased collapsibility of airways. We hypothesized that decreased upstream conductance would be related to inflammation and thickening of the airway walls, increased collapsibility would be related to decreased airway cartilage volume, and decreased collapsibility to inflammation and thickening of the airway walls. Lung tissue was obtained from 72 patients with different degrees of COPD, who were operated upon for a solitary peripheral lung lesion. Maximal flow-static recoil (MFSR) plots to estimate upstream resistance and airway collapsibility were derived in 59 patients from preoperatively measured maximal expiratory flow-volume and pressure-volume curves. In 341 transversely cut airway sections, airway size, airway wall dimensions and inflammatory changes were measured. Airflow obstruction correlated with lung elastic recoil and the MFSR estimate of airway conductance but not to airway collapsibility or to the amount of airway cartilage. The upstream conductance decreased as the inner wall became thicker. Airway collapsibility did not correlate with the amount of airway cartilage, inflammation, or airway wall thickness. We conclude that the maximal flow-static recoil model does not adequately reflect the collapsibility of the flow-limiting segment.