Modeling experiments in animal models of chronic obstructive pulmonary disease

Summary

Chronic obstructive pulmonary disease (COPD) is a chronic bronchitis and/or emphysema characterized by airflow obstruction, which is a highly valued and widely researched disease due to its high incidence and serious impact on patients' ability to work and quality of life. In order to facilitate the study of COPD, the present method is based on the establishment of a rat model of chronic bronchitis, using sulfur dioxide (SO2) inhalation method, and the experimental model of COPD was established by detecting the lung function of the model animals and confirming the occurrence of airflow obstruction.

Principle

The basic principle of the COPD animal modeling experiment is to establish a rat model of chronic bronchitis by _SO2 inhalation, test the function of the model rats, and establish a COPD experimental model by confirming the occurrence of airflow obstruction.

Inhalation of _SO2 produces a decrease in peak expiratory flow rate and an increase in intra-airway pressure per unit of time, i.e., the presence of airflow obstruction.

Operation method

Modeling experiments in animal models of chronic obstructive pulmonary disease

Principle

The basic principle of the COPD animal modeling experiment is to establish a rat model of chronic bronchitis by SO2 inhalation, test the function of the model rats, and establish an experimental model of COPD by confirming the occurrence of airflow obstruction. SO2 inhalation produces a decrease in peak expiratory flow rate and an increase in intra-airway pressure per unit of time, i.e., the presence of airflow obstruction.

Materials and Instruments

Equipment:
① Male Wistar rats, etc.

Move

The basic procedure of animal modeling experiments for chronic obstructive pulmonary disease (COPD) can be divided into the following steps:
A. Healthy male Wistar rats, weighing 150-200 g. The experimental rats were exposed to 250 x ^10-5 _SO2 gas for 5 h/d and 5 d/week for 7 weeks.
B

. Lung function tests: peak expiratory flow rate (PEF,) PEF) and tidal volume (Vt) were decreased, and the intratracheal pressure slope (IP slope) was increased. It can be shown that animals inhaling _SO2 can produce a decrease in peak expiratory flow rate and an increase in intra-airway pressure per unit of time, i.e., the presence of airflow obstruction. If 80% of the mean PEF is used as a cutoff, then >80% means no airflow obstruction, and <80% means airflow obstruction; the former can be regarded as COPD, and the latter is still chronic bronchitis.

Pathomorphologic changes: In rats, there were a large number of mucus plugs and inflammatory cell exudation in the lumen of all levels of bronchial tubes; airway mucosa was degenerated, necrotic, vesiculated, and ulcerated, with epithelial cell hyperplasia, laminarization, and significant proliferation of cup cells, which were also seen in the epithelium of the mucosa of the terminal fine bronchi. The submucosa and periphery of the fine bronchi were infiltrated with a large number of inflammatory cells, predominantly lymphocytes, and the airway smooth muscle was thickened. The alveolar walls were thinned, the alveolar lumen was enlarged and partially ruptured and fused to form pulmonary pustules, and the number of alveoli was significantly reduced.

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