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1 Department of Biomedical Engineering, Boston University, Boston, MA, USA
2 Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: bsuki{at}bu.edu.
Enlargement of the respiratory airspaces is associated with the breakdown and re-organization of the connective tissue fiber network during the development of pulmonary emphysema. In this study, a mouse (C57BL/6) model of emphysema was developed by direct instillation of 1.2 IU of porcine pancreatic elastase (PPE) and compared with control mice treated with saline. The PPE-treatment caused 95% alveolar enlargement (P = 0.001) associated with a 29% lower elastance along the quasi-static pressure-volume curves (P < 0.001). Respiratory mechanics were measured at several positive end-expiratory pressures in the closed chest condition. The dynamic tissue elastance was 19% lower (P < 0.001), hysteresivity was 9% higher (P < 0.05), and harmonic distortion, a measure of collagen-related dynamic nonlinearity, was 33% higher in the PPE-treated group (P < 0.001). Whole lung hydroxyproline content, which represents the total collagen content, was 48% higher (P < 0.01), and 
-elastin content was 13% lower (P = 0.16) in the PPE-treated group. There was no significant difference in airway resistance (P = 0.7). The failure stress at which isolated parenchymal tissues break during stretching was 40% lower in the PPE-treated mice (P = 0.002). These findings suggest that following elastolytic injury, abnormal collagen remodeling may play a significant role in all aspects of lung functional changes leading to progressive emphysema.
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