动物造模,急性肺损伤 zi-bio 2024-03-19 560

　　Objective: To establish a rat model of acute lung injury induced by smoke inhalation from ship fires using multiple composite materials as combustibles and temperature control

　　Method: Design independent smoke production boxes and cabin simulation boxes, and confine conscious rats to designated areas inside the cabin simulation box. During the experiment, the amount of smoke entering the test box is detected and controlled to achieve stable injury factors. The experiment is divided into two parts. The first part is different smoke inhalation time groups, and the survival rate of each group after 48 hours of smoke inhalation is observed; The second part is to select smoke inhalation for 30 minutes as the causative factor, and detect changes in blood gas analysis, lung injury pathological score, alveolar lavage fluid, peripheral blood white blood cells, major inflammatory factors, major signaling factors in signaling pathways, and liver and kidney function at 6 and 24 hours after smoke inhalation

　　Result: 1) The survival rate of different smoke inhalation time groups was 84.21% (15 minute group); 25% (30min group), 0 (50min group); (2) After 30 minutes of smoke inhalation, the levels of carboxyhemoglobin, partial pressure of carbon dioxide, and lactate significantly increased within 1 hour of smoke inhalation (P<0.05), and gradually returned to normal levels thereafter; Compared with the control group, the lung injury score (LIS) and protein content in alveolar lavage fluid (BALF) significantly increased at 6 and 24 hours after smoke inhalation; The total number of white blood cells in BALF significantly increased after smoke inhalation, with the proportion of alveolar macrophages showing a trend of first decreasing and then increasing, while neutrophils showed a trend of first increasing and then decreasing. Studies on various inflammatory factors and signaling pathways have found that activation of multiple signaling factors can occur within 1 hour of smoke inhalation, with WB and immunofluorescence showing the most significant activation at 6 hours and gradually decreasing at 24 hours. There is no specific change in liver and kidney function after smoke inhalation

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