脓毒症休克致急性呼吸窘迫综合征大鼠肺组织肾素——血管紧张素系统的表达变化  

THE EXPRESSION OF RAS IN ARDS RAT LUNG TISSUE INDUCED BY SEPSIS SHOCK

作　　者：白静[1] 张军伟[1] 王建军[1] 王宝华[1] 张文丽[2] 

机构地区：[1]河北联合大学附属医院重症医学科,河北省唐山市063000 [2]河北联合大学医学实验研究中心

出　　处：《中国煤炭工业医学杂志》2014年第10期1661-1664,共4页Chinese Journal of Coal Industry Medicine

摘　　要：目的通过观察脓毒症休克所致急性呼吸窘迫综合征(acute respiratory distress syndrome,ARDS)大鼠肺组织ACE、AngⅡ、Ang(1-7)的表达变化,探讨肾素-血管紧张素系统(renin-angiotensin system,RAS)在脓毒症休克致ARDS中的作用,从而为ARDS的治疗探索新的途径。方法采用盲肠结扎加穿孔(CLP)法建立脓毒症休克致ARDS模型,Western blot测肺组织ACE蛋白的表达及肺组织AngⅡ、Ang(1-7)表达;并测定肺组织湿干重比、血气氧分压(PaO2)及氧合指数(PaO2/FiO2)、肺组织SOD活性及MDA的含量;观察肺组织病理改变。结果与假手术组比较,脓毒症休克致ARDS大鼠肺组织ACE、AngⅡ表达升高,Ang(1-7)表达降低,血气氧分压及氧合指数明显下降,SOD活性降低,MDA含量增加(P<0.05);肺组织病理学观察ARDS大鼠肺间质毛细血管扩张、充血,肺间质和肺泡腔内可见大量液体渗出、炎细胞聚集。结论脓毒症休克致ARDS与RAS激活有关,ACE、AngⅡ可能通过氧化应激途径引起肺损伤,Ang(1-7)可能对肺损伤起到保护作用。Objective To explore the the role of renin angiotensin system to ARDS induced by sepsis shock and find new way for the treatment of ARDS by observe the changes of expression of ACE,AngⅡ,Ang（1-7）in the ARDS rats lung induced by sepsis shock.Methods Cecal ligation and puncture method was adopted to established the ARDS model caused by sepsis shock.After the ARDS models was successfully established,western blotting was used to investigate the protein expression of lung tissue ACE,the lung tissue AngⅡ and Ang（1-7）.Wet dry weight ratio,oxygen partial pressure（PaO2）and oxygenation index（PaO2/FiO2）were measured,as well as activities of SOD and MDA in lung tissue.The changes of lung tissue pathomorphology by HE were observed through the microscope.Results The expression of ACE and AngⅡ of lung tissue in sepsis shock to ARDS rat were much higher than that in sham group at 20 hours after cecal ligation and puncture（P〈0.05）,but the Ang（1-7）of lung tissue in sepsis shock to ARDS rat was much lower（P〈0.05）.The oxygen partial pressure and oxygenation index in sepsis shock to ARDS rat decreased significantly in each time as compared with sham group（P〈0.05）.The activity of SOD in sepsis shock to ARDS rat was much lower than the sham group（P〈0.05）,but the MDA content was much higher（P〈0.05）.The capillary expansion,congestion,large amounts of fluid and inflammatory cell aggregation could be seen in the pulmonary interstitial and alveolar cavity.Conclusions ARDS caused by sepsis shock associates with RAS activation.ACE,AngⅡ may be caused lung injury by oxidative stress.Ang（1-7）can protect lung injury.

关 键 词：脓毒症休克 急性呼吸窘迫综合征 肾素-血管紧张素系统 氧化应激 大鼠 

分 类 号：R631.4[医药卫生—外科学]