Effects of post-treatment with dezocine on acute lung injury caused by intestinal ischemia-reperfusion in rats

  Objective: To investigate the effect of post-treatment with dezocine on acute lung injury caused by intestinal ischemia-reperfusion in rats and its possible mechanism.

  Methods: Thirty-two healthy adult male SD rats were selected and divided into 4 groups by random number table method: CON group was sham operation group; intestinal ischemia-reperfusion model was prepared in Ⅱ/R group; Dez group was transfemored after 1 h of ischemia Dezocine 3 mg 0.6 mL was injected intravenously and reperfused for 1 hour; the 5-HD group was intraperitoneally injected with sodium 5-hydroxydecanoate 10 mg/kg 30 minutes before ischemia, and then the intestinal ischemia-reperfusion model was prepared. Dez group. Immediately after 1 hour of reperfusion, part of the intestinal tissue was taken to observe the morphology of the intestinal mucosa and score the intestinal mucosal injury; the left lung tissue was taken to observe the lung tissue morphology and score the lung injury; the right lung tissue was taken to determine the content of malondialdehyde and MDA. Oxidative dismutase SOD activity and myeloperoxidase MPO activity. Arterial blood was taken to detect serum levels of TNF-a and IL-6.

  Results: Dezocine post-treatment can alleviate the damage to the lungs of the distant organs caused by intestinal ischemia-reperfusion, reduce the scores of intestinal mucosal injury and lung injury, reduce the content of malondialdehyde MDA in lung tissue, and disproportionate superoxide. The activity of enzyme SOD increased, the activity of myeloperoxidase MPO decreased, and the concentration of serum TNF-a and IL-6 decreased significantly. Treatment with mitochondrial ATP-sensitive potassium channel inhibitor 5-hydroxydecanoate can attenuate the protective effect of dezocine on lung injury.

  Conclusion: Dezocine post-treatment can improve the damage of intestinal ischemia-reperfusion in rats to the lungs of the distant organs. Activation of mitochondrial ATP-sensitive potassium channels may be one of the protective mechanisms.