乌司他丁对急性呼吸窘迫综合征保护作用的实验研究

Experimental study of the protective effects of Ulinastatin on acute respiratory distress syndrome

目的探讨乌司他丁治疗急性呼吸窘迫综合征(ARDS)的作用机制。方法将30只Wistar大鼠采用随机数字方法分为空白组、模型组和乌司他丁(UTI)组,由大鼠尾静脉注射油酸0.17 mL/kg复制ARDS病理模型。模型复制成功后2 h、12 h分别予以下干预:UTI组予以UTI 1 064 IU/100 g尾静脉注射,空白组及模型组以生理盐水代替。观察24 h后各组动物的动脉血气、血清超氧化物歧化酶(SOD)、丙二醛(MDA)、肺湿干质量比等指标的变化以及肺脏形态学的改变。结果UTI组血气分析、血清SOD、MDA、肺湿干质量比等指标与对照组比较均有显著性差异(P<0.05或0.01),肺脏组织结构破坏较模型组轻,出血、粒细胞浸润和水肿均少于模型组。结论UTI对油酸型ARDS大鼠有治疗作用,其机制可能与增强机体抗自由基能力,抑制急性肺损伤炎症递质和细胞因子释放相关。

Objective It is to explore the mechanism of Ulinastatin on（UTI）acute respiratory distress syndrome（ARDS）. Methods Thirty Wistar rats were randomly divided into three groups： normal group, model group, UTI group. A rat model of ARDS was established by injection of oleic acid with 0.17 mL/kg. After the models were successfully established for 2 h and 12 h, the following interventions were performed on： UTI group was given UTI 1 064 IU/100 g by injecting in caudal vein, normal group and model group was given normal saline instead. The changes of arterial blood gas, serum concentration. of SOD and MDA, lung wet dry ratios, and pathologic alteration of lung were observed. Results There were significant differences in arterial blood gas, SOD, MDA level and lung wet dry ratios between UTI group and other two groups （P 〈 0.01 or 0.05）. Compared with that in model group, damage of lung tissue structure was lighter, and hemorrhage, granulocyte infiltration, edema was less. Conclusion UTI has a treatment function on rats with ARDS of oleic acid, and the mechanism may be that it can strengthen anti-oxygen radicals ability and inhibit the releasing of mediators of inflammation and cytokine of acute lung injury.