ARDS-5号对大鼠油酸型急性呼吸窘迫综合征的影响

Study of ARDS-5 on oleic acid-induced acute respiratory distress syndrome rats

目的:探讨ARDS-5号治疗急性呼吸窘迫综合征(ARDS)的作用及其机理。方法:将40只Wistar大鼠,采用随机数字方法分空白组、模型组、乌司他丁组(UTI)、ARDS-5号组(中药组),各组10只;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:乌司他丁(UTI)组予以UTI尾静脉注射,生理盐水灌胃;ARDS-5号组予以ARDS-5号中药灌胃、生理盐水尾静脉注射;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SOD与MDA等指标的变化以及肺脏形态学的改变。结果:ARDS-5号组及乌司他丁组动物动脉血气分析、血清SOD与MDA等指标,与模型组比较均有显著差异(P<0.05～0.01),肺脏组织结构破坏较模型组轻,出血、粒细胞浸润和水肿均轻于模型组。结论:ARDS-5号能改善油酸型ARDS大鼠通气情况,提高血氧含量,增强SOD活力,抑制MDA释放,其机理可能与抑制炎性介质的释放,增强机体抗自由基能力相关。

Objective： To investigate the effects and the probable mechanisms of ARDS-5 treating in oleic acid （OA） induced acute respiratory distress syndrome （ARDS） on rats. Methods： Rat model of ARDS was established by injection of OA with 0. 17 ml/kg. Forty Wistar rats were randomly divided into the normal group, OA group, Ulinastatin （UTI） group and ARDS-5 group, with 10 rats in each group. The following in the models were examined： arterial blood gas, serum concentrations of SOD, MDA, patholog- ic alteration of lung. Results： （1） Arterial blood gas, PO2 in OA group were significantly lower, which was quite different from other groups （P d0.01）, PCO2 was superior than other groups （P 〈0.05） ,and there were no differences in other three groups （P 〉0.05）. （2） SOD level： in OA group, it decreased sig nificantly; but there was little degression in UTI group and ARDS-5 group; in OA group, MDA level in- creased significantly （P d0.01）, and both UTI and ARDS-5 groups were similar to the normal group （P 〉0.05）. （3） The pathologic manifestation of lung was significantly altered; UTI group and ARDS-5 could lighten the alteration. Conclusions： After OA injection, the increase of MDA level resulted in a series of pathophysiologic alteration, which might aggravate lung injury. This process might be an important link to the pathogentic mechanism of ARDS by OA. This study suggests that the utilization of ARDS-5 can pre- vent the increasing of MDA and make the SOD level increase. It may be one of the mechanisms against OA-induced ARDS.