动物造模,致急性肺损伤大鼠模型 z-bio 2022-11-03 367

　　Objective: To establish a rat model of acute lung injury (ALI) induced by smoke inhalation from ship fire with multiple composite materials as combustor and temperature controlled

　　Methods: An independent smoke producing box and a compartment simulation box were designed, and conscious rats were confined to the cage in the designated area of the compartment simulation box. During the experiment, the aim of stabilizing the injury factors was achieved by detecting and controlling the amount of smoke in the test box. The experiment was conducted in two parts. The first part was the different smoke inhalation time groups, and the survival rate of each group after smoke inhalation for 48 hours was observed; The second part is to select smoke inhalation for 30 minutes as the injury factor, and detect the changes of blood gas analysis, pathological score of lung injury, alveolar lavage fluid, peripheral white blood cells, major inflammatory factors, major signal factors in the signal pathway, liver and kidney functions 6 and 24 hours after smoke inhalation

　　Results: 1) The survival rate of different smoke inhalation time groups was 84.21% (15 min group); 25% (30min group), 0 (50min group); (2) The values of carboxyhemoglobin, partial pressure of carbon dioxide and lactic acid increased significantly within 1h after smoke inhalation 30min (P<0.05), and then gradually returned to normal levels; Compared with the control group, the lung injury score (LIS) and the protein content in alveolar lavage fluid (BALF) were significantly increased 6 and 24 hours after smoke inhalation; The total number of white blood cells in BALF increased significantly after smoke inhalation, in which the proportion of alveolar macrophages decreased first and then increased, while neutrophils increased first and then decreased. Research on a variety of inflammatory factors and signal pathways found that a variety of signal factors could be activated within 1h of smoke inhalation, WB and immunofluorescence showed the most significant activation within 6h, and gradually decreased within 24h. There was no specific change in liver and kidney functions after smoke inhalation

　　Conclusion: A stable, reliable and highly lethal model of simulated smoke inhalation lung injury in ship fire has been established. In the acute phase of smoke inhalation, there are extensive activation of multiple inflammatory pathways, accompanied by typical inflammatory cell changes and lung injury characteristics, which can lay a foundation for further research