动物造模 z-bio 2022-09-09 854

　　Objective: To investigate the effect and possible mechanism of dezocine postconditioning on acute lung injury induced by intestinal ischemia-reperfusion in rats.

　　METHODS: Thirty-two healthy adult male SD rats were selected and divided into 4 groups by random number table method: CON group was the sham operation group; Intravenous injection of dezocine 3 mg 0.6 mL, reperfusion for 1 h; 5-HD group was intraperitoneally injected with sodium 5-hydroxydecanoate 10 mg/kg 30 min before ischemia, and then the intestinal ischemia-reperfusion model was established. Dez group. Immediately after 1 h of reperfusion, part of the intestinal tissue was taken to observe the intestinal mucosal morphology and score the intestinal mucosal injury; the left lung tissue was taken to observe the lung tissue morphology and score the lung injury; Oxide dismutase SOD activity and myeloperoxidase MPO activity, arterial blood was collected to detect the levels of TNF-a and IL-6 in serum.

　　RESULTS: Dezocine post-treatment could alleviate the damage of distant organs and lungs caused by intestinal ischemia-reperfusion, reduce the intestinal mucosal injury score and lung injury score, and reduce the content of malondialdehyde (MDA) and superoxide disproportionation in lung tissue. The enzyme SOD activity increased, the myeloperoxidase MPO activity decreased, and the serum TNF-a and IL-6 concentrations decreased significantly. The protective effect of dezocine on lung injury was attenuated by treatment with sodium 5-hydroxydecanoate, a mitochondrial ATP-sensitive potassium channel inhibitor.

　　CONCLUSION: Dezocine postconditioning can improve the damage of intestinal ischemia-reperfusion to the lungs of distant organs in rats, and activation of mitochondrial ATP-sensitive potassium channels may be one of the protective mechanisms.