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Updated: May 19, 2026
05:48
Lung Fixation under Constant Pressure for Evaluation of Emphysema in Mice
Published on: September 26, 2019
Acute mechanical forces cause deterioration in lung structure and function in elastase-induced emphysema.
M V Szabari1, H Parameswaran, S Sato
1Dept. of Biomedical Engineering, Boston Univ., Boston, MA 02215, USA.
Summary
Deep inspirations in mice with emphysema induced acute lung structure and function changes, creating a potential model for acute exacerbations of chronic obstructive pulmonary disease (AECOPD). This study offers a new avenue for AECOPD research.
Area of Science:
- Pulmonary Medicine
- Biomedical Engineering
- Animal Models
Background:
- The relationship between chronic obstructive pulmonary disease (COPD) progression and exacerbations remains poorly understood.
- A critical gap exists in the lack of a reliable animal model for acute exacerbations of COPD (AECOPD).
Purpose of the Study:
- To investigate the impact of mechanical forces from deep inspirations (DIs) on short-term lung deterioration.
- To establish a potential animal model that mimics AECOPD.
Main Methods:
- Elastase-treated mice were subjected to ventilation with or without DIs at varying time points post-treatment.
- Lung function was assessed using body plethysmography and forced oscillations.
- Histological analysis quantified airspace diameters, alveolar wall thickness, septal ruptures, and airway attachment density.
Main Results:
- Deep inspirations significantly altered lung function parameters (FRC, compliance, resistance, hysteresivity) in emphysematous mice.
- At 21 days post-elastase treatment, DIs induced structural changes including increased alveolar wall thickness and septal ruptures, and decreased airway attachment density.
- These functional and structural changes mimicked key aspects of AECOPD.
Conclusions:
- Acute mechanical forces, such as DIs, can induce irreversible lung damage and functional impairment in emphysematous lungs once critical remodeling has occurred.
- The application of DIs in mice with established emphysema presents a promising and viable model for studying AECOPD.
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