舒芬太尼后处理对子宫缺血-再灌注大鼠急性肺损伤的影响

目的研究舒芬太尼后处理对子宫缺血-再灌注(IR)大鼠急性肺损伤的影响。方法成年雌性SD大鼠45只,随机分为三组:对照组(C组)、IR组和舒芬太尼后处理组(SPC组),每组15只。IR组、SPC组建立子宫缺血45 min再灌注2 h模型,SPC组给予舒芬太尼后处理。检测大鼠处理后子宫、血清及肺组织中TNF-α、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性以及肺湿干重比(W/D)、肺通透性指数(LPI)。结果 IR组、SPC组子宫、血浆及肺脏中TNF-α、MDA含量、W/D、LPI明显高于C组(P0.05);SPC组TNF-α、MDA含量、W/D、LPI明显低于IR组(P0.05);IR组、SPC组子宫、血浆以及肺脏中SOD活性明显低于C组(P0.05);SPC组SOD活性明显高于IR组(P0.05)。结论舒芬太尼后处理能减轻子宫缺血-再灌注大鼠急性肺损伤,可能与减少氧自由基和炎症因子的产生,降低肺通透性,减轻肺水肿,从而减轻子宫缺血-再灌注大鼠引发的急性肺损伤有关。

Effect of sufentanil postconditioning on acute lung injury induced by ischemia-reperfusion of uterine in rats

Objective To investigate the effect of sufentanil postconditioning on acute lung in-jury induced by ischemia-reperfusion of uterine in rats.Methods Fourty-five adult female Sprague-Dawley rats were randomly divided into 3 groups(n = 1 5 each):control group (group C),ischemia-reperfusion group (group IR)and sufentanil postconditioning group(group SPC).Group SPC received sufentanil 10 μg/kg via intraperitoneal injection before inducing reperfusion of uterine.Ischemia-reper-fusion of uterine was produced by occlusion of bilateral uterine arteries for 45 min followed by reper-fusion for 2 h in group IR and group SPC.Then the content of tumor necrosis factor-α(TNF-α),mal-odiadehyde (MDA)and superoxide dismutase (SOD)activity were measured in uterus,serum and lung tissue,lung wet to dry weight ratio (W/D),lung permeability index (LPI)were compared. Results Compared with group C,TNF-α,MDA content,W/D and LPI in uterus,serum and lung tissue were significantly increased in group IR and group SPC(P <0.05).TNF-α,MDA content,W/D and LPI in uterus,serum and lung tissue were significantly attenuated in group SPC as compared with group IR (P <0.05 ).Compared with group C,SOD activity in uterus,serum and lung tissue was significantly attenuated in group IR and group SPC (P <0.05).SOD in uterus,serum and lung tissue were significantly increased in group SPC as compared with group IR (P < 0.05 ). Conclusion Sufentanil postconditioning attenuates pulmonary injury caused by ischemia-reperfusion of uterine in rats by inhibiting the inflammatory reaction and suppressing the activation of oxyradical.