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目的探讨μ阿片受体激动剂DAMGO对创伤-内毒素二次打击所致大鼠急性肺损伤的影响。方法 SD成年大鼠32只,随机分为正常对照组(N组)、空白对照组(B组)、DAMGO组(D组)和DAMGO+μ阿片受体拮抗剂CTOP组(DC组)。采用双侧股骨中段闭合性骨折6h后腹腔注射脂多糖(Lipopolysaccharides,LPS)5 mg/kg造模。N组只麻醉不造模,B组造模15min后腹腔注射等量生理盐水,D组注射DAMGO 200 μg/kg,DC组注射CTOP 600 μg/kg,5 min后注射DAMGO200 μg/kg。药物注射6h后行动脉血气分析,观察并比较肺组织病理改变,检测肺组织干湿重比、肿瘤坏死因子-α(TNF-α)、IL-6、丙二醛(MDA)的含量及超氧化物歧化酶(SOD)活性。结果二次打击后大鼠肺功能降低,肺组织出现了明显炎症反应。与D组比较,B、DC组动脉血PaO2、pH值明显降低;肺组织Smith评分明显升高(P<0.05);肺组织干湿重比明显降低(P<0.05);肺组织MDA、TNF-α、IL-6含量明显升高(P<0.05),SOD活性明显降低(P<0.05)。结论μ阿片受体激动剂DAMGO对创伤-内毒素二次打击所致大鼠急性肺损伤有一定保护作用。
Objective To investigate the effect of μ opioid receptor agonist DAMGO on acute lung injury induced by traumatic-endotoxin secondary shock in rats. Methods Thirty SD adult rats were randomly divided into normal control group (N group), blank control group (B group), DAMGO group (D group) and DAMGO + μ opioid receptor antagonist CTOP group (DC group). Six-hour occlusion of bilateral femoral fractures was induced by intraperitoneal injection of lipopolysaccharides (LPS) 5 mg / kg. Rats in group A were injected with DAMGO 200 μg / kg intraperitoneally at 15 min after injection of DAMGO. Groups in control group received CTOP 600 μg / kg and group D 200 μg / kg after 5 min. Arterial blood gas was analyzed 6h after drug injection. The pathological changes of lung tissue were observed and compared. The dry weight ratio, the content of tumor necrosis factor-α (TNF-α), IL-6 and malondialdehyde (MDA) Oxide dismutase (SOD) activity. Results The rat lung function was decreased after the second strike, and the lung tissue showed obvious inflammatory reaction. Compared with group D, PaO2 and pH of arterial blood in group B and DC decreased obviously; the score of Smith in lung tissue increased significantly (P <0.05); the ratio of wet to dry weight in lung tissue decreased significantly (P <0.05); the content of MDA and TNF (P <0.05), and the activity of SOD decreased obviously (P <0.05). Conclusion μ-opioid receptor agonist DAMGO has a protective effect on acute lung injury induced by traumatic-endotoxin secondary shock in rats.