中华心律失常学杂志
中華心律失常學雜誌
중화심률실상학잡지
CHINESE JOURNAL OF CARDIAC ARRHYTHMIAS
2011年
5期
363-368
,共6页
任淑静%金奇%周建%林长坚%庞旸%张凝%凌天佑%顾刚%沈永初%陈颖%陆林%吴立群
任淑靜%金奇%週建%林長堅%龐旸%張凝%凌天祐%顧剛%瀋永初%陳穎%陸林%吳立群
임숙정%금기%주건%림장견%방양%장응%릉천우%고강%침영초%진영%륙림%오립군
粒细胞-集落刺激因子%缺血再灌注%再灌注心律失常%心室颤动%除颤阈值
粒細胞-集落刺激因子%缺血再灌註%再灌註心律失常%心室顫動%除顫閾值
립세포-집락자격인자%결혈재관주%재관주심률실상%심실전동%제전역치
Granulocyte cdong-stimulating factor%Ischemia reperfusion%Reperfusion arrhythmia%Ventricular fibrillation%Defibrillation threshold
目的 探讨静脉用粒细胞集落刺激因子(granulocyte colony-stimulating factor,G-CSF)对家兔缺血再灌注心肌是否有急性保护作用,既能否增加心肌保护性蛋白磷酸化-丝氨酸/苏氨酸蛋白激酶( phosphorylation-Akt,p-Akt)的表达及是否具有抑制室性心律失常作用.方法 14只家兔随机平均分为2组(G-CSF组和对照组,n=7).所有家兔均开胸结扎冠状动脉左前降支30min,再灌注4 h(G-CSF组再灌注同时静脉泵G-CSF 10 μg/kg维持30 min,对照组静脉用生理盐水10 mL/kg维持30 min).利用60道袜套状电极进行双心室整体心外膜电生理标测.两组分别于基础状态下,缺血时及再灌注4h后通过程序性电刺激诱发心室颤动(VF),并测定除颤阈值(defibrillation threshold,DFT).通过快速傅里叶转换技术测定每个标测电极的VF激动频率.应用Curtis-Walker评分系统评价两组再灌注4h内室性心律失常发生情况.ELISA法测定血清肿瘤坏死因子α(TNF-α)和白细胞介素-10(IL-10)的浓度,蛋白质印迹(Western Blot)测定缺血区心肌p-Akt的表达水平.结果 所有家兔均可通过程序性电刺激诱发出稳定VF.与对照组相比,G-CSF显著降低了再灌注室性心律失常分数[(6.3±1.5)对(2.3±2.6),P=0.038].两组间基础状态下、缺血及再灌注时DFT及VF激动频率差异无统计学意义(P＞0.05).两组再灌注4h后VF激动频率较基础状态及缺血时降低,差异有统计学意义(P＜0.05).G-CSF不增加血清TNF-α及IL-10的浓度,但可增加缺血区心肌P-Akt的表达.结论 静脉用G-CSF未改变VF激动频率及缺血再灌注DFT,但是G-CSF通过增加缺血区心肌组织中p-Akt的表达可减少心肌损伤,减少再灌注心律失常.研究结果提示静脉使用G-CSF对缺血再灌注心肌具有一定的急性保护作用.
目的 探討靜脈用粒細胞集落刺激因子(granulocyte colony-stimulating factor,G-CSF)對傢兔缺血再灌註心肌是否有急性保護作用,既能否增加心肌保護性蛋白燐痠化-絲氨痠/囌氨痠蛋白激酶( phosphorylation-Akt,p-Akt)的錶達及是否具有抑製室性心律失常作用.方法 14隻傢兔隨機平均分為2組(G-CSF組和對照組,n=7).所有傢兔均開胸結扎冠狀動脈左前降支30min,再灌註4 h(G-CSF組再灌註同時靜脈泵G-CSF 10 μg/kg維持30 min,對照組靜脈用生理鹽水10 mL/kg維持30 min).利用60道襪套狀電極進行雙心室整體心外膜電生理標測.兩組分彆于基礎狀態下,缺血時及再灌註4h後通過程序性電刺激誘髮心室顫動(VF),併測定除顫閾值(defibrillation threshold,DFT).通過快速傅裏葉轉換技術測定每箇標測電極的VF激動頻率.應用Curtis-Walker評分繫統評價兩組再灌註4h內室性心律失常髮生情況.ELISA法測定血清腫瘤壞死因子α(TNF-α)和白細胞介素-10(IL-10)的濃度,蛋白質印跡(Western Blot)測定缺血區心肌p-Akt的錶達水平.結果 所有傢兔均可通過程序性電刺激誘髮齣穩定VF.與對照組相比,G-CSF顯著降低瞭再灌註室性心律失常分數[(6.3±1.5)對(2.3±2.6),P=0.038].兩組間基礎狀態下、缺血及再灌註時DFT及VF激動頻率差異無統計學意義(P＞0.05).兩組再灌註4h後VF激動頻率較基礎狀態及缺血時降低,差異有統計學意義(P＜0.05).G-CSF不增加血清TNF-α及IL-10的濃度,但可增加缺血區心肌P-Akt的錶達.結論 靜脈用G-CSF未改變VF激動頻率及缺血再灌註DFT,但是G-CSF通過增加缺血區心肌組織中p-Akt的錶達可減少心肌損傷,減少再灌註心律失常.研究結果提示靜脈使用G-CSF對缺血再灌註心肌具有一定的急性保護作用.
목적 탐토정맥용립세포집락자격인자(granulocyte colony-stimulating factor,G-CSF)대가토결혈재관주심기시부유급성보호작용,기능부증가심기보호성단백린산화-사안산/소안산단백격매( phosphorylation-Akt,p-Akt)적표체급시부구유억제실성심률실상작용.방법 14지가토수궤평균분위2조(G-CSF조화대조조,n=7).소유가토균개흉결찰관상동맥좌전강지30min,재관주4 h(G-CSF조재관주동시정맥빙G-CSF 10 μg/kg유지30 min,대조조정맥용생리염수10 mL/kg유지30 min).이용60도말투상전겁진행쌍심실정체심외막전생리표측.량조분별우기출상태하,결혈시급재관주4h후통과정서성전자격유발심실전동(VF),병측정제전역치(defibrillation threshold,DFT).통과쾌속부리협전환기술측정매개표측전겁적VF격동빈솔.응용Curtis-Walker평분계통평개량조재관주4h내실성심률실상발생정황.ELISA법측정혈청종류배사인자α(TNF-α)화백세포개소-10(IL-10)적농도,단백질인적(Western Blot)측정결혈구심기p-Akt적표체수평.결과 소유가토균가통과정서성전자격유발출은정VF.여대조조상비,G-CSF현저강저료재관주실성심률실상분수[(6.3±1.5)대(2.3±2.6),P=0.038].량조간기출상태하、결혈급재관주시DFT급VF격동빈솔차이무통계학의의(P＞0.05).량조재관주4h후VF격동빈솔교기출상태급결혈시강저,차이유통계학의의(P＜0.05).G-CSF불증가혈청TNF-α급IL-10적농도,단가증가결혈구심기P-Akt적표체.결론 정맥용G-CSF미개변VF격동빈솔급결혈재관주DFT,단시G-CSF통과증가결혈구심기조직중p-Akt적표체가감소심기손상,감소재관주심률실상.연구결과제시정맥사용G-CSF대결혈재관주심기구유일정적급성보호작용.
Objective The aim of this study is to determine whether granulocyte colony-stimulating factor (G-CSF) has acute protection on myocardial ischemia reperfusion injury in rabbit heart by increasing the expression of phosphorylation-Akt,and thus,decreases the incidence of ventricular arrhythmias.Methods In the fourteen open-chest rabbits,left anterior descending coronary artery (LAD) was occluded for 30 minutes followed by 4 hours of reperfusion.Rabbits were randomly assigned into the following two groups:( 1 ) G-CSF group:intravenously administrating G-CSF ( 10 μg/kg) for 30 minutes ; (2) control group:intravenously administrating normal saline from the onset of reperfusion.A sock containing 60 electrodes was placed over the entire ventricular epicardium for electrical mapping.Ventricular fibrillation (VF) was induced and defibrillation threshold (DFT) was determined and compared at baseline,ischemia and reperfusion stage between the two groups.The activation rate was estimated by Fast Fourier Transform analysis of VF at each electrode.Curtis and Walker Arrhythmia Scoring system was used to evaluate the reperfusion ventricular arrhythmia among the 4 hours of reperfusion.The serum concentration of TNF-α and IL-10 were measured by ELISA.The expression of p-Akt was evaluated by western blot analysis in the myocardial ischemic zone.Results VF can be induced by programmed electrical stimulation in each rabbit.Compared to control,G-CSF significantly reduced the arrhythmia score[ (6.3±1.5)vs.(2.3±2.6),P=0.038].The DFT and VF activation rate were not significantly different at baseline,ischemia and reperfusion stage between the two groups ( P＞0.05).Compared to the baseline and ischemia stage,the activation rate of VF decreased obviously at the reperfusion stage ( P＜0.05 ).The blood concentration of TNF-α and IL-10 were not changed,but P-Akt was more strongly activated in the ischemic zone by intravenously administrating G-CSF.Conclusion Intravenous administration of G-CSF didn' t change neither the peak frequency of VF nor the DFT,but it can ameliorate myocardial ischemia reperfusion injury by reducing reperfusion ventricular arrhythmia and increasing the expression of p-Akt.The results of this study indicated that intravenous administration of G-CSF could have some acute cardioprotective effect on myocardial ischemia reperfusion injury in rabbits.
