Objective To explore dezocine post conditioning on acute lung injury induced by intestinal ischemia and reperfusion induced in rats. Methods According to the random number seed, the healthy male SD rats were randomly divided into 4 groups:Rats in Control group (CON group) were subjected to separate the superior mesenteric artery without being obstructed. Rats in intestinal ischemia-reperfusion group (Ⅱ/R group) were set intestinal ischemia-reperfusion model and administered saline 0.6 mL intravenously after occlusion. In dezocine post conditioning group (Dez group)rats were administered dezocine 0.6 mL 3 mg intravenously after occlusion. In 5-hydroxydecanoate sodium group (5-HD group) rats were administered 5-hydroxydecanoate sodium (10 mg/kg) by peritoneal injection 30min before occlusion then operated as group Dez. The animals were killed at 1 h of reperfusion with the intestinal tissue removed to calculate the index of quantitative assessment of intestinal mucous membrane injury. Tissues of left lung were obtained for observation of histopathology with light microscope and the index of quantitative assessment of histologic lung injury was calculated. The concentrations of malondialdehyde (MDA), superoxide dismutase (SOD) activation and myeloperoxidase level in each group were detected via tissues of left lung. The concentrations of TNF-a and IL-6 were also examined. Results Acute lung injury induced by intestinal ischemia and reperfusion induced in rats was improved by dezocine post conditioning. Chiu score, lung injure score, malondialdehyde (MDA) content, myeloperoxidase(MPO) level and the concentrations of TNF-a and IL-6 were descended while superoxide dismutase (SOD) activation was rised. The protective effects of dezocine post conditioning were attenuated by injecting 5-hydroxydecanoate sodium via peritoneal cavity which was a selective mitochondrial ATP-sensitive potassium channel antagonist. Conclusions Dezocine post-conditioning protects against lung injury induced by intestinal ischemia-reperfusion in rats. One of the protective effects may be related to opening mitochondrial ATP-sensitive potassium channel.