Morphogenesis of pulmonary damage in lipopolysaccharide-induced acute aspiration bronchopneumonia
Keywords:
lipolysaccharide, experimental pneumonia, morphogenesisAbstract
Background. The morphogenesis of pulmonary injury during coronavirus (SARS-CoV-2) infection has not been fully established, which dictates the need for experimental reproduction of the key pathogenetic mechanisms of acute respiratory distress syndrome (ARDS) and pulmonary fibrosis. Objective. To study the morphogenesis of pulmonary injury during the development of lipopolysaccharide-induced acute aspiration bronchopneumonia in experiment. Methods. To simulate pneumonia in Wistar rats (n=29), in compliance with bioethical standards, one and two days before the operation, a solution of lipopolysaccharide (LPS; "MEDGAMAL") was injected intraperitoneally at a dose of 25 mg/100 g of body weight. During the operation, a sterile nylon thread and 50 μl of LPS solution at a dose of 1.25 mg/100 g of body weight were injected endotracheally. On 1st, 3rd, 5th, 7th and 14th days, 3 animals were taken out of the experiment. Serial paraffin sections were stained with hematoxylin and eosin; examined and photographed. Results. Mortality within 14 days was 44.8%; the animals had cyanosis, distant wheezing, crepitation symptom. Within an hour after the administration of LPS, hyperimmune inflammation was formed with the development of ARDS. In the future, the damage of the vessels of the microvasculature, the lung parenchyma, in the form of areas of emphysema with ruptures of the interalveolar membranes with their pronounced leukocytic infiltration and the development of hemorrhagic pneumonia on the 3rd day progressed. Signs of purulent inflammation appeared on the 5th day in the form of purulent peribronchial abscesses. From 5-7 days, reactive hyperplasia of lymphoid follicles, active fibrosis of the bronchi and pulmonary parenchyma, and vascular hyalinosis were noted. On the 14th day, there were signs of chronic productive inflammation with the development of pulmonary fibrosis and vascular sclerosis. Conclusion. Comparison of the obtained data with those available in the literature makes it possible to draw a certain analogy between the development of this model of bronchopnemonia and the development of a pathological process in the lungs during SARS-CoV-2 infection.
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