title: Physiological and morphological determinants of maximal expiratory flow in chronic obstructive lung disease.
abstract: 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.
authors.affiliation: Dept of Pediatrics, Erasmus University, Rotterdam, The Netherlands.
authors.forename: H A
authors.initials: HA
authors.lastname: Tiddens
authors.forename: J M
authors.initials: JM
authors.lastname: Bogaard
authors.forename: J C
authors.initials: JC
authors.lastname: de Jongste
authors.forename: W C
authors.initials: WC
authors.lastname: Hop
authors.forename: H O
authors.initials: HO
authors.lastname: Coxson
authors.forename: P D
authors.initials: PD
authors.lastname: Paré
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000403:Airway Resistance / Q000502:physiology; D001980:Bronchi / Q000473:pathology / Q000503:physiopathology; D001991:Bronchitis / Q000473:pathology / Q000503:physiopathology; D002356:Cartilage / Q000473:pathology; D005260:Female; D005541:Forced Expiratory Volume / Q000502:physiology; D005652:Functional Residual Capacity / Q000502:physiology; D006801:Humans; D007320:Inspiratory Capacity / Q000502:physiology; D008168:Lung / Q000473:pathology / Q000503:physiopathology; D008170:Lung Compliance / Q000502:physiology; D008173:Lung Diseases, Obstructive / Q000503:physiopathology*; D008297:Male; D008449:Maximal Expiratory Flow-Volume Curves / Q000502:physiology*; D008875:Middle Aged; D011014:Pneumonia / Q000473:pathology / Q000503:physiopathology; D011312:Pressure; D001261:Pulmonary Atelectasis / Q000473:pathology / Q000503:physiopathology; D012115:Residual Volume / Q000502:physiology; D014109:Total Lung Capacity / Q000502:physiology; D014797:Vital Capacity / Q000502:physiology