Objective To establish rat models of chronic obstructive pulmonary disease (COPD) and study the pathological characteristics of airflow obstruction Method SO 2 inhalation method was used to establish rat models After exposure to SO 2 for 7 weeks, peak expiratory flow (PEF), peak inspiratory flow (PIF), intratracheal pressure (IP) and IP slope in rat were measured by Maclab data recording and analysis system Experimental rats with PEF less than 80% of the mean of the normal rats were classified as airflow obstructed, while those with PEF greater than 80% of mean of normal rats were non obstructed Pathological changes in airway and lung tissue were compared between these two groups Result In experimental animals, PEF was significantly decreased ( P <0 005) and IP slope increased ( P <0 001) as compared with normal rats Epithelial damage, goblet cell hyperplasia and inflammatory cell infiltration in cartilaginous bronchi were more remarkable in experimental rats with airflow obstruction than those without airflow obstruction ( P <0 001, <0 01, <0 001, respectively) Furthermore, pathological changes in airway lumen, epithelium and airway wall in membranous and respiratory bronchioles were more marked in experimental rats with airflow obstruction than those without airflow obstruction ( P <0 001 or P <0 05) There was a negative correlation between PEF values and epithelial hyperplasia, goblet cell hyperplasia, inflammatory cell infiltration, smooth muscle hyperplasia and mucous plug in membranous and respiratory bronchioles ( P <0 001 or P <0 05) Conclusion SO 2 inhalation may cause chronic bronchitis with airflow obstruction, i e COPD in rats COPD was induced in 64% (16 of 25) of the experimental group rats Objective To establish rat models of chronic obstructive pulmonary disease (COPD) and study the pathological characteristics of airflow obstruction Method SO 2 inhalation method was used to establish rat models after exposure to SO 2 for 7 weeks, peak expiratory flow (PEF), peak inspiratory flow (PIF), intratracheal pressure (IP) and IP slope in rat were measured by Maclab data recording and analysis system Experimental rats with PEF less than 80% of the mean of the normal rats were classified as airflow obstructed, while those with PEF greater than 80% of mean of normal rats were non obstructed Pathological changes in airway and lung tissue were compared between these two groups Result In experimental animals, PEF was significantly decreased (P <0 005) and IP slope increased compared with normal rats Epithelial damage, goblet cell hyperplasia and inflammatory cell infiltration in cartilaginous bronchi were more remarkabl e in experimental rats with airflow obstruction than those without airflow obstruction (P <0 001, <0 01, <0 001, respectively) Furthermore, pathological changes in airway lumen, epithelium and airway wall in membranous and respiratory bronchioles were more marked in experimental rats with airflow obstruction than those without airflow obstruction (P <0 001 or P <0 05) There was a negative correlation between PEF values ​​and epithelial hyperplasia, goblet cell hyperplasia, inflammatory cell infiltration, smooth muscle hyperplasia and mucous plug in membranous and respiratory Conclusions SO 2 inhalation may cause chronic bronchitis with airflow obstruction, ie COPD was induced in 64% (16 of 25) of the experimental group rats (P <0 001 or P <0 05)