组织源性血管紧张素Ⅱ在败血症休克中的作用

The role of tissue-derived angiotensin (AGT) Ⅱ in septic shock

为探讨组织源性血管紧张素Ⅰ(AGT-Ⅱ)在败血症休克发病中的作用,本文在结扎大鼠盲肠加穿孔(CLP)的败血症模型上观察早期(10h)、晚期(20h)败血症大鼠主动脉、心肌组织的AGT-Ⅱ含量、血糖和组织脂质过氧化产物(MDA)水平变化及AGT-Ⅱ转换酶抑制剂(ACEI)Captopril对其影响。结果表明,败血症休克时主动脉、心肌AGT-Ⅱ均显著升高,在早期败血症时比假手术对照组分别增加51%、133%(P<0.01),在晚期败血症时分别增加53%、30%(P<0.05)。心肌、肝组织MDA含量在早、晚期败血症时均显著升高(P<0.01)。灌胃Captopril可以维持败血症大鼠血糖、动脉压水平,降低组织AGT-Ⅱ含量及MDA水平。提示,组织源性AGT-Ⅱ在败血症休克的发病中具有重要意义,应用ACEI防治是有益的。

In order to investigate the pathogenetic role of tissue-derived AGT Ⅰ in septic shock, the changes of AGT Ⅱ in aorta and heart were observed on early(10h) and late septic shock model produced by cecal ligature and puncture (CLP) in rats. Results showed that AGT Ⅱ contents in aorta and heart were significantly elevated during early and late sepsis. The increases of AGT Ⅱ contents during early and late sepsis are 51%, 53%(in aorta) and 132%, 30%(in heart)respectively compared to shamanimals (P<0.01). The MDA contents of myocardium and liver in CLP animals increased significantly during early (147% and 57% respectively, P<0.01) and late (197% and 114%, respectively, P<0.01) sepsis. Administration of captopril(10mg/kg/day, oral for 2 days) reduced the tissue levels of AGT Ⅱ and MDA contents dramatical ly in late septic shock. It also maintained blood pressure and plasma glucose at nearly normal levels. The results suggested that tissue AGT Ⅱ plays an important role in the pathogenesis of septic shock and captopril had beneficial effects on septic shock.