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J Appl Physiol 98: 503-511, 2005. First published October 1, 2004; doi:10.1152/japplphysiol.00590.2004
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Mechanics, nonlinearity, and failure strength of lung tissue in a mouse model of emphysema: possible role of collagen remodeling

Satoru Ito,1 Edward P. Ingenito,2 Kelly K. Brewer,1 Lauren D. Black,1 Harikrishnan Parameswaran,1 Kenneth R. Lutchen,1 and Béla Suki1

1Department of Biomedical Engineering, Boston University, Boston; and 2Division of Pulmonary and Critical Care Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts

Submitted 14 June 2004 ; accepted in final form 27 September 2004

Enlargement of the respiratory air spaces is associated with the breakdown and reorganization 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 {alpha}-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, after elastolytic injury, abnormal collagen remodeling may play a significant role in all aspects of lung functional changes and mechanical forces, leading to progressive emphysema.

elastance; extracellular matrix; failure stress; resistance


Address for reprint requests and other correspondence: B. Suki, Dept. of Biomedical Engineering, Boston Univ., 44 Cummington St., Boston MA 02215 (E-mail: bsuki{at}bu.edu)




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