心电与循环
心電與循環
심전여순배
Journal of Electrocardiology(China)
2014年
3期
229-232
,共4页
程俊华%洪俊%郑程%陈学思%陈星星%赵景琳%李进%林加锋
程俊華%洪俊%鄭程%陳學思%陳星星%趙景琳%李進%林加鋒
정준화%홍준%정정%진학사%진성성%조경림%리진%림가봉
心室起搏%电重构%ERK1/2磷酸化
心室起搏%電重構%ERK1/2燐痠化
심실기박%전중구%ERK1/2린산화
Ventricular pacing%Electrical remodeling%ERK1/2 phosphorylation
目的:探讨右心室心尖部起搏对Beagle犬心室肌电重构及细胞外信号调节激酶(ERK)1/2磷酸化水平的影响。方法成年雄性Beagle犬12只,年龄3~4年,体重20~24kg,随机分为对照组(n=6)和起搏组(n=6),均植入DDD起搏器后程控至关闭状态,起搏组术后1周时开启起搏器并使心室起搏最大化。于术前及术后1周、4周关闭起搏器后行心电图及超声心动描记术检查,术后4周时处死动物,观察心肌病理结果,采用免疫印迹法检测犬右心室心肌总ERK1/2及其磷酸化水平的变化。结果两组心室肌病理及超声心动描记术、心率、QRS时间、总ERK1/2的表达差异均无统计学意义(均P>0.05);与对照组相比,术后4周时起搏组Tp- e间期、Q- T间期均增大,p- ERK增多(均P<0.05)。结论右心室心尖部起搏可以导致心肌复极延长及促进心肌ERK1/2的磷酸化。
目的:探討右心室心尖部起搏對Beagle犬心室肌電重構及細胞外信號調節激酶(ERK)1/2燐痠化水平的影響。方法成年雄性Beagle犬12隻,年齡3~4年,體重20~24kg,隨機分為對照組(n=6)和起搏組(n=6),均植入DDD起搏器後程控至關閉狀態,起搏組術後1週時開啟起搏器併使心室起搏最大化。于術前及術後1週、4週關閉起搏器後行心電圖及超聲心動描記術檢查,術後4週時處死動物,觀察心肌病理結果,採用免疫印跡法檢測犬右心室心肌總ERK1/2及其燐痠化水平的變化。結果兩組心室肌病理及超聲心動描記術、心率、QRS時間、總ERK1/2的錶達差異均無統計學意義(均P>0.05);與對照組相比,術後4週時起搏組Tp- e間期、Q- T間期均增大,p- ERK增多(均P<0.05)。結論右心室心尖部起搏可以導緻心肌複極延長及促進心肌ERK1/2的燐痠化。
목적:탐토우심실심첨부기박대Beagle견심실기전중구급세포외신호조절격매(ERK)1/2린산화수평적영향。방법성년웅성Beagle견12지,년령3~4년,체중20~24kg,수궤분위대조조(n=6)화기박조(n=6),균식입DDD기박기후정공지관폐상태,기박조술후1주시개계기박기병사심실기박최대화。우술전급술후1주、4주관폐기박기후행심전도급초성심동묘기술검사,술후4주시처사동물,관찰심기병리결과,채용면역인적법검측견우심실심기총ERK1/2급기린산화수평적변화。결과량조심실기병리급초성심동묘기술、심솔、QRS시간、총ERK1/2적표체차이균무통계학의의(균P>0.05);여대조조상비,술후4주시기박조Tp- e간기、Q- T간기균증대,p- ERK증다(균P<0.05)。결론우심실심첨부기박가이도치심기복겁연장급촉진심기ERK1/2적린산화。
Objective To investigate the effects of right ventricular apical pacing on electrical remodeling and ERK1/2 phosphorylation in beagle myocardium. Methods 12 male beagles, 3- 4 years old, underwent DDD pacemaker implanta-tion and were randomly divided into two groups (n=6). The pacemakers were turned on and programmed to ensure ventric-ular pacing 1 week after implantation in pacing group and turned off al the time in control group. The ECG and UCG were recorded before, 1 and 4 weeks after procedure with the pacemaker turned off. The beagles were sacrificed 4 weeks after procedure and phosphorylated ERK1 / 2 of right ventricular myocardium was determined by Western blotting. Results There was no statistical difference in the expression of ERK1 / 2, heart rate, QRS duration, BNP, ventricular myocardial pathology and parameters of UCG between the two groups. Tpeak- Tend interval and QT duration were prolonged and the expression of phosphorylated ERK1/2 increased in pacing group compared with control group(P<0.05) 4 weeks after pro-cedure. Conclusion Right ventricular apical pacing may induce myocardial repolarization prolongation and promote ERK1/2 phosphorylation of myocardium.