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外源性一氧化碳分子对脓毒症时心脏炎症反应的抑制作用及机制
引用本文:王波,仇雪枫,孙炳伟,孙艳,陈曦. 外源性一氧化碳分子对脓毒症时心脏炎症反应的抑制作用及机制[J]. 临床急诊杂志, 2011, 12(6): 369-372
作者姓名:王波  仇雪枫  孙炳伟  孙艳  陈曦
作者单位:江苏大学附属医院创伤中心 江苏镇江,212001
基金项目:国家自然科学基金(No:30772256,81071546); 江苏省自然科学基金面上项目(No:BK2008237); 江苏省政府留学基金(No:2008-K002); 江苏省“333工程”科研基金(No:2010-75)
摘    要:目的:探讨外源性一氧化碳释放分子2(CORM-2)对脓毒症时心脏炎症反应的抑制作用和心脏功能的影响。方法:将45只雄性BALB/c小鼠按随机数字表法分为假手术组、盲肠结扎和穿孔术(CLP)组和CLP+CORM-2组。CLP+CORM-2组除伤后使用CORM-2外,其他处理同CLP组。于伤后24h检测小鼠血清天门冬氨酸氨基转移酶(AST)和乳酸脱氢酶(LDH)水平;用流式细胞术检测心肌细胞凋亡率;同时用彩色多普勒超声成像系统进行心脏超声检查。结果:与假手术组比较,24hCLP组血浆AST、LDH的水平明显增加,心肌细胞凋亡率明显增高,心脏超声检查显示LVEF、LVFS均显著低于假手术组(P<0.05);CLP+CORM-2组AST、LDH的水平降低,心肌细胞凋亡率明显下降,心脏超声检查显示LVEF、LVFS均显著提高(P<0.05)。结论:外源性CORM-2能明显抑制脓毒症心脏炎症反应,降低心肌细胞凋亡率,提高左室泵血能力,从而有效防止脓毒症时心肌损伤,提高心脏功能。

关 键 词:脓毒症  一氧化碳  心肌  超声  凋亡

Inhibitive effect of carbon monoxide-releasing molecules 2 on the inflammation of heart in septic mice
WANG Bo , QIU Xuefeng , SUN Bingwei , SUN Yan , CHEN Xi. Inhibitive effect of carbon monoxide-releasing molecules 2 on the inflammation of heart in septic mice[J]. Journal of Clinical Emergency Call, 2011, 12(6): 369-372
Authors:WANG Bo    QIU Xuefeng    SUN Bingwei    SUN Yan    CHEN Xi
Affiliation:WANG Bo QIU Xuefeng SUN Bingwei SUN Yan CHEN Xi(1Department of Trauma Center,the Affiliated Hospital,Jiangsu University,Zhenjiang 212001,China)
Abstract:Objective:To explore the inhibitive effects and potential mechanisms of carbon monoxide-releasing moleculesⅡ on the inflammation of heart in septic mice.Method:Forty-five BALB/c male mice were randomly divided into sham,CLP,and CLP +CORM-2(with 8 mg/kg CROM-2) . The serum samples from each group were collected at 24 h post CLP. The serum levels of AST and LDH were examined. Apoptosis of cardiac tissue were examined and apoptosis index(AI) was calculated. The evaluation of heart function with Agilent Sonos 5 500 color Doppler imaging system in identifying post-CLP myocardial condition were performed.Result:The serum levels of AST and LDH,AI of myocardial tissue in CLP mice increased significantly(P0.05) . Compared with those of CLP group,the above index were decreased in CLP+CROM-2 group(P0.05) . In parallel,the levels of LVEF、LVFS in CORM-2-treated CLP mice were significantly increased compared with CLP group(P0.05) .Conclusion:Taken together these findings indicate that CORM-released CO upregulates the heart function in sepsis. This effect of CORM might be one underlying mechanism explaining its inhibition of inflammation and apoptosis in sepsis.
Keywords:sepsis  carbon monoxide  myocardial  apoptosis  color doppler imaging system  
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