中国综合临床
中國綜閤臨床
중국종합림상
CLINICAL MEDICINE OF CHINA
2010年
12期
1271-1273
,共3页
陈协辉%李鹏%黄小平%王东明%陈宋明%杨泽民%陈智凡%许文敏%陈丽萍
陳協輝%李鵬%黃小平%王東明%陳宋明%楊澤民%陳智凡%許文敏%陳麗萍
진협휘%리붕%황소평%왕동명%진송명%양택민%진지범%허문민%진려평
硫化氢心肌%缺血再灌注%心律失常%ATP敏感性钾通道%信号传导
硫化氫心肌%缺血再灌註%心律失常%ATP敏感性鉀通道%信號傳導
류화경심기%결혈재관주%심률실상%ATP민감성갑통도%신호전도
Hydrogen sulfide%Myocardial ischemia reperfusion%Ventricular arrhythmia%ATP sensitive potassium channel%Signal transduction
目的 研究气体信号分子硫化氢(H2S)对大鼠心肌缺血再灌注损伤的保护作用.方法 以硫化氢钠作为H2S供体,建立心肌缺血再灌注损伤动物模型,将实验大鼠按随机原则分为假手术组(对照组)、心肌缺血再灌注组(I/R组)、H2S+I/R组(H2S组)及H2S+K-ATP通道阻断剂glibenclamide+I/R组(H2S+GLI组),监测大鼠心率、动脉压、左心室内压及收缩、舒张功能等血流动力学指标,观察大鼠室性心律失常的发生情况.结果 在心肌缺血前预先给H2S可明显降低大鼠心肌缺血再灌注室性心律失常的发生率(H2S组66.5%与I/R组33.5%,P＜0.05)以及室性心律失常评分[H2S组(2.6±0.7)分与I/R组(4.5±0.8)分,P＜0.05].提前给予K-ATP通道阻断剂glibenclamide,结果发现H2S的抗心律失常作用减弱[H2S组(2.6±0.7)分与H2S+GLI组(4.0±0.6)分,P＜0.05].结论 H2S具有保护大鼠心肌缺血再灌注损伤的作用,其作用机制可能与细胞内K-ATP通道信号转导途径相关.
目的 研究氣體信號分子硫化氫(H2S)對大鼠心肌缺血再灌註損傷的保護作用.方法 以硫化氫鈉作為H2S供體,建立心肌缺血再灌註損傷動物模型,將實驗大鼠按隨機原則分為假手術組(對照組)、心肌缺血再灌註組(I/R組)、H2S+I/R組(H2S組)及H2S+K-ATP通道阻斷劑glibenclamide+I/R組(H2S+GLI組),鑑測大鼠心率、動脈壓、左心室內壓及收縮、舒張功能等血流動力學指標,觀察大鼠室性心律失常的髮生情況.結果 在心肌缺血前預先給H2S可明顯降低大鼠心肌缺血再灌註室性心律失常的髮生率(H2S組66.5%與I/R組33.5%,P＜0.05)以及室性心律失常評分[H2S組(2.6±0.7)分與I/R組(4.5±0.8)分,P＜0.05].提前給予K-ATP通道阻斷劑glibenclamide,結果髮現H2S的抗心律失常作用減弱[H2S組(2.6±0.7)分與H2S+GLI組(4.0±0.6)分,P＜0.05].結論 H2S具有保護大鼠心肌缺血再灌註損傷的作用,其作用機製可能與細胞內K-ATP通道信號轉導途徑相關.
목적 연구기체신호분자류화경(H2S)대대서심기결혈재관주손상적보호작용.방법 이류화경납작위H2S공체,건립심기결혈재관주손상동물모형,장실험대서안수궤원칙분위가수술조(대조조)、심기결혈재관주조(I/R조)、H2S+I/R조(H2S조)급H2S+K-ATP통도조단제glibenclamide+I/R조(H2S+GLI조),감측대서심솔、동맥압、좌심실내압급수축、서장공능등혈류동역학지표,관찰대서실성심률실상적발생정황.결과 재심기결혈전예선급H2S가명현강저대서심기결혈재관주실성심률실상적발생솔(H2S조66.5%여I/R조33.5%,P＜0.05)이급실성심률실상평분[H2S조(2.6±0.7)분여I/R조(4.5±0.8)분,P＜0.05].제전급여K-ATP통도조단제glibenclamide,결과발현H2S적항심률실상작용감약[H2S조(2.6±0.7)분여H2S+GLI조(4.0±0.6)분,P＜0.05].결론 H2S구유보호대서심기결혈재관주손상적작용,기작용궤제가능여세포내K-ATP통도신호전도도경상관.
Objective To explore the effects and mechanism of hydrogen sulfide on myocardial ischemia reperfusion in rats. Methods With sodium hydrogen sulfide (NaHS) as a donor of hydrogen sulfide ( H2S), we established myocardial ischemia-reperfusion injury model in rats. The SD rats were randomly divided into control group,myocardial ischemia reperfusion group (I/R group), H2S group,and H2S and glibenclamide (H2S + GLI)group. We monitored the hemodynamics index of rats, including heart rate, arterial pressure, left ventricular pressure. The rate of ventrical arrhythmia was also observed in each group. Results H2 S significantly reduced the ventricular arrhythmia (VA) occurrence (H2S group 66.5% vs I/R group 33.5% (P ＜0.05) and score in myocardial ischemia reperfusion rats (H2S group 2. 6 ±0. 7 vs I/R group 4. 5 ±0. 8(P＜0.05). The KATP channel blocker,glibenclamide,could weaken the antiarrhythmic effects of H2S ( H2S group 2. 6 ±0. 7 vs. H2S + GLI group 4. 0 ± 0. 6, P ＜ 0.05 ). Conclusions H2S has the protective effect against myocardial ischemia reperfusion damage. This function may be associated with the KATP signal transduction pathway in cells.
