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  

Inhibitive effect of carbon monoxide-releasing molecules 2 on the inflammation of heart in septic mice

作　　者：王波[1] 仇雪枫[1] 孙炳伟[1] 孙艳[1] 陈曦[1] 

机构地区：[1]江苏大学附属医院创伤中心,江苏镇江212001

出　　处：《临床急诊杂志》2011年第6期369-372,共4页Journal of Clinical Emergency

基　　金：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。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.

关 键 词：脓毒症 一氧化碳 心肌 超声 凋亡 

分 类 号：R631[医药卫生—外科学]