【Animal Modeling】-Animal Model of Chronic Bronchitis

  (1) Modeling experiment Put the mouse in a 10 L lower mouth bottle, leave a 1.5 cm diameter vent on the bottle cap, connect the lower mouth to the tee, and the other end. 50 ml syringe and lighted cigarette. The syringe continuously injects 400 ml of cigarette smoke from the tee tube each time (the smoke concentration in the bottle is about 4%), and smokes for 30 minutes. Smokers smoked once a day in the morning and afternoon for the first 10 days, and once a day for the next 10 days. The entire modeling process takes 20 days and may cause chronic bronchitis in mice.

  (2) Model characteristics According to optical microscope, most model mice have different degrees of chronic inflammatory cells (including lymphocytes, plasma cells, monocytes) and a small amount of neutrophils in the trachea and bronchus, and infiltrate them. Lodging, adhesion and shedding of cilia were found in the epithelium of the bronchial mucosa. Ciliated cells show degeneration, necrosis and shedding. Ciliary cell proliferation and squamous metaplasia can be seen in some animals. The bronchial mucosal epithelial goblet cells increased significantly, the cell body enlarged, and the cytoplasm contained abundant mucin particles. The bronchial lumen contains more secretions, macrophages and polymorphonuclear leukocytes. Significant inflammatory cell infiltration was also found around the small blood vessels associated with the trachea at all levels. In severe cases, it is "sleeved". The alveolar diaphragm is widened, accompanied by inflammatory cell infiltration, telangiectasia and congestion. Bronchiectasis and emphysema were found at the end of the lungs. Electron microscopic observation revealed that the epithelial cilia of each layer of the bronchus were significantly reduced and messy, the "9 + 2" structure of the cilia was blurred, the cytoplasmic electron density was reduced, and some lipid droplets and edema areas appeared. The structure of the nuclear envelope and cell membrane is unknown, and shrinkage can be seen. Mitochondria are swollen, cr loose, and there are even vacuoles. The endoplasmic reticulum expanded, free ribosomes decreased, and a large number of secondary lysosomes were found. Occasional connective tissue hyperplasia occurs in the submucosa of the bronchioles, the alveolar epithelium is slightly damaged, the type I cells are slightly swollen, and the microvilli on the surface of the type II cells are reduced.

  (3) Comparative Medicine Chronic bronchitis generally develops gradually after repeated episodes of acute bronchitis. Smoking methods involve time and quantity, and it is easy to do it later. Whether it is heavy or light, it may promote the formation of early lesions. We also proved that long-term secondhand smoke can cause serious damage to the respiratory tract of mice. The pathological changes observed with light and electron microscopes are very similar to the early pathological changes of human chronic bronchitis. Glandular hyperplasia is unclear because the bronchial glands in mice are underdeveloped. Studies have shown that many components of tobacco smoke, such as carbon monoxide, formaldehyde, acetaldehyde, acrolein, nitric oxide and cyanide, can directly stimulate the airway mucosa and impair its function and form.