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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 investigate the changes of ACE, AngⅡand Ang (1-7) in the lung tissue of acute respiratory distress syndrome (ARDS) induced by septic shock in rats, and to explore the renin-angiotensin system -angiotensin system (RAS) in ARDS induced by septic shock, so as to explore a new way for the treatment of ARDS. Methods The model of sepsis-induced ARDS was established by cecal ligation plus perforation (CLP). The protein expression of ACE and AngⅡ, Ang (1-7) in lung tissue were detected by Western blot. The ratio of wet to dry weight, PaO2 and PaO2 / FiO2, SOD activity and MDA content in lung tissue were measured. Pathological changes of lung tissue were observed. Results Compared with the sham operation group, the expression of ACE, AngⅡ and Ang (1-7) in the lungs of ARDS rats were decreased after septic shock, the partial pressure of oxygen and oxygen in blood gas decreased significantly, the activity of SOD decreased, the content of MDA (P <0.05). Pathological observation of lungs revealed a large amount of fluid exudation and inflammatory cell aggregation in the pulmonary interstitial capillaries in ARDS rats. Conclusions ARDS induced by septic shock is related to the activation of RAS. Angiotensin Ⅱ and angiotensin Ⅱ may induce lung injury through oxidative stress. Ang (1-7) may play a protective role on lung injury.