摘要
目的:观察肾素-血管紧张素系统(RAS)在大鼠急性肺损伤中的作用及地塞米松(DEX)的影响。方法:在大鼠失血性休克的基础上,腹腔注射内毒素(二次打击)造成急性肺损伤模型,直接插管法检测大鼠平均动脉血压(MAP);逆转录聚合酶链式反应(RT-PCR)观察各组大鼠肺脏组织中血管紧张素转换酶(ACE)、血管紧张素原(AGT)、血管紧张素Ⅱ 1型受体(AT1)和血管紧张素Ⅱ 2型受体(AT2)mRNA的表达及测定大鼠血清血管紧张素Ⅰ(AngⅠ)、血管紧张素Ⅱ(AngⅡ)的变化。结果:二次打击组(HL)大鼠平均动脉血压恢复很慢,而地塞米松治疗组(HLD)平均动脉血压恢复的速度较HL明显增快,且平均动脉血压水平的升高具有明显差异。与对照组(C)相比,HL组ACE、AGTmRNA表达水平明显增高,而HLD组明显低于HL组。AT1、AT2 mRNA各组表达水平则无明显差异。与C组相比,HL组AngⅡ的含量明显升高,HLD组大鼠血清AngⅡ的含量比HL组均明显减低,Ang Ⅰ含量的变化不明显。结论:失血性休克后LPS诱发的急性肺损伤可能与激活肺脏的肾素-血管紧张素系统有关,抑制肺脏的肾素-血管紧张素系统的激活是DEX轻这种急性肺损伤的机制之一。
AIM： To explore the relationship between renin - angiotensin system （RAS） and acute lung injury （ALI） in rats, and the effect of dexamethasone （DEX） on RAS was observed. METHODS： The rat model of ALI was induced by hemorrhagic shock and LPS administered intraperitoneally. The changes of MAP and the effects of DEX on MAP were observed. The mRNA expressions of ACE, AGT, AT1 and AT2 in lung tissue were assayed by RT - PCR. The changes of Ang Ⅰ and Ang Ⅱ in the serum and the effects of DEX on them were observed. RESULTS： The increasing of MAP was statistically obvious. MAP in hemorrhagic shock ＋ LPS （HL） group recovered more slowly than that in HL ＋ DEX （HLD） group. ACE, AGT, AT1 and AT2 mRNA expressions in HL group were increased, and higher than those in HLD group. The change of Aug Ⅱ in serum in HL group was obviously higher than that in HLD group, while that of Ang Ⅰ was not obvious. CONCLUSION： ALI activates RAS in rat lung, and promotes the production of Aug Ⅱ then aggravates the injury of lung through increasing the expression of ACE and AGT. DEX decreases expression of Aug Ⅱ.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2009年第1期22-25,共4页
Chinese Journal of Pathophysiology
基金
吉林省科学技术厅资助项目(No.200705152)
