Objective: To establish a rat model of acute lung injury by injecting lipopolysaccharide (LPS) into the trachea, and observe the changes of lung injury over time.
Method: 32 healthy SD rats were randomly divided into normal group and model group, with 8 normal group and 24 model group. The model group was divided into 3 subgroups according to the length of LPS infusion. There were 8 animals in each of the 3-hour group, the 6-hour group, and the 12-hour group. A LPS (2 mg/kg) exposed tracheal instillation was used to replicate the AII rat model. General condition of rats, whole body observation of lungs, lung function test, calculation of lung dry-wet weight ratio, interleukin 1β (IL-1β) and interleukin 8 (IL-8) bronchoalveolar lavage fluid (BALF)), tumor necrosis Factor-α (TNF-α) detection, malondialdehyde (MDA), lung tissue superoxide dismutase (SOD) detection, hematoxylin-eosin staining (HE staining) tissue morphology observation, various evaluations over time Changing conditions of acute lung injury.
Result: After modeling, the survival rate of the rats in the model group was 100. Compared with the normal group, the rats were generally indifferent, eating less, significantly reducing activity, increasing nasal mucus secretion, accelerating breathing rate, and wheezing. The general observation of the lung showed that the lung tissues of the left and right hilum of the 3-hour group had liver-like changes, the left and right lobes were scattered at the bleeding points, and the bleeding site was bright red. Pulmonary functions include forced vital capacity in 0.1 seconds (FEV0.1), forced vital capacity in 0.3 seconds (FEV0.3), and forced vital capacity in 3 hours (FVC) (FEV0.1/FVC; FEV0). . Rat group .3/FVC) significantly decreased (Pu003c0.05.Pu003c0.01) and lung dry-wet weight ratio significantly increased (Pu003c0.01); IL-1β, IL- content 8, BALF TNF-α Significantly increased (Pu003c0.01), MDA content significantly increased (Pu003c0.01), SOD content significantly decreased (Pu003c0.01); HE staining showed clear alveolar separation. Lung thickening, interstitial edema and red blood cell exudation.
Conclusion: Exposure to tracheal infusion of LPS can cause significant deterioration of rat lung function, severe lung inflammation, oxidation-antioxidant imbalance, severe pulmonary edema, pulmonary hemorrhage, and can cause acute lung injury.