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肠淋巴液引流对失血性休克小鼠心肌组织ACE/ACE2的作用
引用本文:王紫监,刘俊芬,蒋丽娜,张立民,刘桂青,王淮淮,赵自刚,牛春雨. 肠淋巴液引流对失血性休克小鼠心肌组织ACE/ACE2的作用[J]. 中国应用生理学杂志, 2017, 33(1): 61-65. DOI: 10.12047/j.cjap.5448.2017.015
作者姓名:王紫监  刘俊芬  蒋丽娜  张立民  刘桂青  王淮淮  赵自刚  牛春雨
作者单位:1. 河北北方学院微循环研究所, 张家口 075000;2. 河北北方学院附属第二医院, 宣化 075100;3. 河北北方学院附属第一医院, 张家口 075000
基金项目:河北北方学院创新人才培育基金(CXRC1314)
摘    要:目的:观察失血性休克后小鼠心肌组织血管紧张素转换酶(ACE)/ACE2平衡的变化及肠淋巴液引流(PHSML)的作用。方法:BALB/c雄性小鼠24只,随机分为对照组、假手术组、休克组、休克+引流组(n=6)。建立失血性休克模型,行液体复苏;休克+引流组液体复苏后,引流肠淋巴液。在液体复苏后6 h或假手术组相应时间点、对照组于麻醉后,留取心肌组织,qRT-PCR法检测ACE、ACE2、血管紧张素Ⅱ (Ang Ⅱ)1型受体(AT1R)、Mas相关G蛋白偶联受体(Mas1R)的mRNA表达,ELISA方法检测Ang Ⅱ和Ang (1-7)含量。结果:休克组小鼠心肌组织ACE与AT1R mRNA表达、Ang Ⅱ水平均显著高于对照组与假手术组,ACE2与Mas1R mRNA表达显著低于对照组与假手术组、Ang (1-7)含量显著低于对照组,ACE/ACE2、Ang Ⅱ/Ang (1-7)、AT1R/Mas1R显著高于对照组与假手术组;PHSML引流显著抑制了失血性休克对这些指标的作用。结论:失血性休克上调心肌ACE-Ang Ⅱ-AT1R轴、下调ACE2-Ang (1-7)-Mas1R轴表达,引起ACE/ACE2失衡;PHSML引流下调ACE-Ang Ⅱ-AT1R轴、上调ACE2-Ang (1-7)-Mas1R轴表达,在一定程度上维持了ACE/ACE2平衡。

关 键 词:失血性休克  肠淋巴液  引流术  心肌  血管紧张素转换酶  小鼠  
收稿时间:2015-12-14

Role of mesenteric lymph drainage in the balance of ACE/ACE2 in murine myocardium following hemorrhagic shock
WANG Zi-jian,LIU Jun-fen,JIANG Li-na,ZHANG Li-min,LIU Gui-qing,WANG Huai-huai,ZHAO Zi-gang,NIU Chun-yu. Role of mesenteric lymph drainage in the balance of ACE/ACE2 in murine myocardium following hemorrhagic shock[J]. Chinese journal of applied physiology, 2017, 33(1): 61-65. DOI: 10.12047/j.cjap.5448.2017.015
Authors:WANG Zi-jian  LIU Jun-fen  JIANG Li-na  ZHANG Li-min  LIU Gui-qing  WANG Huai-huai  ZHAO Zi-gang  NIU Chun-yu
Affiliation:1. Institute of Microcirculation of Hebei North University, Zhangjiakou 075000;2. the Second Affiliated Hospital of Hebei North University, Xuanhua 075100;3. the First Affiliated Hospital of Hebei North University, Zhangjiakou 075000, China
Abstract:Objective: To observe the change of angiotensin converting enzyme (ACE) and ACE2 in the murine myocardium followed hemorrhagic shock and the role of post-hemorrhagic shock mesenteric lymph (PHSML) drainage.Methods: Twenty-four male mice were ran-domly divided into control, sham, shock, and shock + drainage groups. A hemorrhagic shock model was established and then fluid resuscita-tion was performed to the mice in the shock and shock + drainage groups, and the PHMSL was drained in the shock + drainage group after fluid resuscitation. After 6 h of resuscitation in the shock and shock + drainage groups or corresponding time in the sham group, or after anesthesia in the control group, the myocardial tissues were harvested for the determination of the mRNA expressions of ACE, ACE2, angiotensin Ⅱ (Ang Ⅱ) type 1 receptor (AT1R), and Mas related G protein coupled receptor (Mas1R) using the method of qRT-PCR, and the levels of Ang Ⅱ and Ang (1-7) using the method of ELISA.Results: In the myocardial tissue of shock group, the ACE and AT1R mRNA expressions and Ang Ⅱ level were significantly increased than those of the control and sham groups, the ACE2 and Mas1R mRNA expressions were significantly de-creased than that of the control and sham groups, the Ang (1-7) level was decreased compared with the control group, the ratios of ACE/ACE2, Ang Ⅱ/Ang (1-7), and AT1R/Mas1R in the shock group were significantly increased than the control and sham groups. Meanwhile, PHSML drainage obviously suppressed the effects of hemorrhagic shock on these indices.Conclusion: Hemorrhagic shock up-regulated the ACE-Ang Ⅱ-AT1R axis, down-regulated the ACE2-Ang (1-7)-Mas1R axis, and induced the unbalance of ACE and ACE2 in myocardial tis-sue. PHSML drainage decreased the ACE-Ang Ⅱ-AT1R axis and increased the ACE2-Ang (1-7)-Mas1R axis, resulted in the balance of ACE and ACE2.
Keywords:hemorrhagic shock  mesenteric lymph  drainage  myocardium  angiotensin converting enzyme  mouse  
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