动物造模,吸入致急性肺损伤大鼠模型 z-bio 2022-09-14 474

　　Objective: To establish a temperature-controllable rat model of acute lung injury induced by ship fire smoke inhalation using various composite materials as combustion materials.

　　Methods: Design an independent smoke-producing box and a cabin simulation box, and confine the awake rats to the rat cage in the designated area of the cabin simulation box. During the experiment, the smoke intake in the test box was detected and controlled to achieve a stable injury factor. Objective. The experiment is divided into two parts. The first part is for different smoke inhalation time groups to observe the survival rate of each group after smoke inhalation for 48 hours; the second part is to select smoke inhalation for 30 minutes as the injury factor, and analyze the blood gas at 6 and 24 hours after smoke inhalation. , Lung injury pathological score, bronchoalveolar lavage fluid, peripheral blood leukocytes, major inflammatory factors, major signaling factors in signaling pathways, and changes in liver and kidney function were detected.

　　Results: 1) The survival rate results of different smoke inhalation time groups were: 84.21% (15min group); 25% (30min group), 0 (50min group); (2) 1h carboxyhemoglobin, carbon dioxide partial pressure, carbon dioxide partial pressure, 1h after smoke inhalation 30min The lactate value increased significantly within 1 hour after smoke inhalation (P<0.05), and then gradually returned to normal levels; ) protein content increased significantly; the total number of leukocytes in BALF increased significantly after smoke inhalation, and the proportion of alveolar macrophages first decreased and then increased, while neutrophils first increased and then decreased. The study of signaling pathways found that the activation of various signaling factors occurred within 1 hour of smoke inhalation, and WB and immunofluorescence showed that the activation was most significant at 6 hours, and gradually decreased after 24 hours. There was no specific change in liver and kidney function after smoke inhalation.

　　CONCLUSION: A stable, reliable and high lethal lung injury model was established to simulate ship fire smoke inhalation. 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. It can lay the foundation for further in-depth research.