国际麻醉学与复苏杂志
國際痳醉學與複囌雜誌
국제마취학여복소잡지
INTERNATIONAL JOURNAL OF ANESTHESIOLOGY AND RESUSCITATION
2013年
2期
115-121
,共7页
温传允%张冯江%钱令波%朱曼华%严敏
溫傳允%張馮江%錢令波%硃曼華%嚴敏
온전윤%장풍강%전령파%주만화%엄민
利多卡因%七氟烷%后处理%心肌保护%Bcl-2
利多卡因%七氟烷%後處理%心肌保護%Bcl-2
리다잡인%칠불완%후처리%심기보호%Bcl-2
Lidocaine%Sevoflurane%Postconditioning%Cardioprotection%Bcl-2
目的 研究利多卡因对七氟烷后处理心肌保护作用的影响,并探讨其可能的机制.方法 采用Langendorff装置平衡灌注20 min后,全心停灌40 min,再灌注120 min,建立雄性Sprague-Dawley大鼠离体心脏缺血/再灌注(ischemia/reperfusion,I/R)模型.采用随机数字表法将大鼠心脏随机分为7组(每组6只):假手术(Sham)组、I/R组、I/R+20mg/L利多卡因(I/R+Lid-20)组、七氟烷后处理(sevoflurane postconditioning,SPC)组、七氟烷后处理+2、10 mg/L或20 mg/L利多卡因(SPC+Lid-2、SPC+Lid-10、SPC+Lid-20)组.连续监测左室发展压(left ventricular developing pressure,LVDP)、舒张末压(left ventricular end-diastolic pressure,LVEDP)、心率(heart rate,HR)、左室内压上升/下降最大速率(maximal rise/fall rate of left ventricular pressure,±dp/dtmax)以及冠脉流量(coronary artery flow,CF).于再灌注5min和10 min时,收集冠脉流出液测定乳酸脱氢酶(lactate dehydrogenase,LDH)和肌酸激酶(creatine kinase,CK)的活性.于再灌注末测定心肌梗死面积及相关蛋白的表达.结果 与I/R组比较,SPC组、SPC+Lid-2组以及SPC+Lid-10组的LVDP、dp/dtmax和CF均明显升高,LVEDP、LDH和CK活性、心肌梗死面积[(23.9±1.4)％,(20.5±1.3)％,(24.7±2.1)％vs(47.9±3.3)％]均明显降低(P＜0.05)；而I/R+Lid-20组、SPC+Lid-20组的各指标与I/R组比较,差异无统计学意义(P＞0.05); SPC组上调了心肌磷酸化的Akt (phosphoralated-Akt,p-Akt)、磷酸化的细胞外信号调节激酶1/2(phosphoralated-extracellular regulated kinase1/2,p-Erk1/2)以及Bcl-2的表达(P＜0.05vsI/R组),而20mg/L的利多卡因抑制了SPC对心肌Bcl-2表达的上调作用. 结论 20 mg/L的利多卡因取消了SPC的心肌保护作用,此效应可能与抑制Bcl-2蛋白表达有关.
目的 研究利多卡因對七氟烷後處理心肌保護作用的影響,併探討其可能的機製.方法 採用Langendorff裝置平衡灌註20 min後,全心停灌40 min,再灌註120 min,建立雄性Sprague-Dawley大鼠離體心髒缺血/再灌註(ischemia/reperfusion,I/R)模型.採用隨機數字錶法將大鼠心髒隨機分為7組(每組6隻):假手術(Sham)組、I/R組、I/R+20mg/L利多卡因(I/R+Lid-20)組、七氟烷後處理(sevoflurane postconditioning,SPC)組、七氟烷後處理+2、10 mg/L或20 mg/L利多卡因(SPC+Lid-2、SPC+Lid-10、SPC+Lid-20)組.連續鑑測左室髮展壓(left ventricular developing pressure,LVDP)、舒張末壓(left ventricular end-diastolic pressure,LVEDP)、心率(heart rate,HR)、左室內壓上升/下降最大速率(maximal rise/fall rate of left ventricular pressure,±dp/dtmax)以及冠脈流量(coronary artery flow,CF).于再灌註5min和10 min時,收集冠脈流齣液測定乳痠脫氫酶(lactate dehydrogenase,LDH)和肌痠激酶(creatine kinase,CK)的活性.于再灌註末測定心肌梗死麵積及相關蛋白的錶達.結果 與I/R組比較,SPC組、SPC+Lid-2組以及SPC+Lid-10組的LVDP、dp/dtmax和CF均明顯升高,LVEDP、LDH和CK活性、心肌梗死麵積[(23.9±1.4)％,(20.5±1.3)％,(24.7±2.1)％vs(47.9±3.3)％]均明顯降低(P＜0.05)；而I/R+Lid-20組、SPC+Lid-20組的各指標與I/R組比較,差異無統計學意義(P＞0.05); SPC組上調瞭心肌燐痠化的Akt (phosphoralated-Akt,p-Akt)、燐痠化的細胞外信號調節激酶1/2(phosphoralated-extracellular regulated kinase1/2,p-Erk1/2)以及Bcl-2的錶達(P＜0.05vsI/R組),而20mg/L的利多卡因抑製瞭SPC對心肌Bcl-2錶達的上調作用. 結論 20 mg/L的利多卡因取消瞭SPC的心肌保護作用,此效應可能與抑製Bcl-2蛋白錶達有關.
목적 연구리다잡인대칠불완후처리심기보호작용적영향,병탐토기가능적궤제.방법 채용Langendorff장치평형관주20 min후,전심정관40 min,재관주120 min,건립웅성Sprague-Dawley대서리체심장결혈/재관주(ischemia/reperfusion,I/R)모형.채용수궤수자표법장대서심장수궤분위7조(매조6지):가수술(Sham)조、I/R조、I/R+20mg/L리다잡인(I/R+Lid-20)조、칠불완후처리(sevoflurane postconditioning,SPC)조、칠불완후처리+2、10 mg/L혹20 mg/L리다잡인(SPC+Lid-2、SPC+Lid-10、SPC+Lid-20)조.련속감측좌실발전압(left ventricular developing pressure,LVDP)、서장말압(left ventricular end-diastolic pressure,LVEDP)、심솔(heart rate,HR)、좌실내압상승/하강최대속솔(maximal rise/fall rate of left ventricular pressure,±dp/dtmax)이급관맥류량(coronary artery flow,CF).우재관주5min화10 min시,수집관맥류출액측정유산탈경매(lactate dehydrogenase,LDH)화기산격매(creatine kinase,CK)적활성.우재관주말측정심기경사면적급상관단백적표체.결과 여I/R조비교,SPC조、SPC+Lid-2조이급SPC+Lid-10조적LVDP、dp/dtmax화CF균명현승고,LVEDP、LDH화CK활성、심기경사면적[(23.9±1.4)％,(20.5±1.3)％,(24.7±2.1)％vs(47.9±3.3)％]균명현강저(P＜0.05)；이I/R+Lid-20조、SPC+Lid-20조적각지표여I/R조비교,차이무통계학의의(P＞0.05); SPC조상조료심기린산화적Akt (phosphoralated-Akt,p-Akt)、린산화적세포외신호조절격매1/2(phosphoralated-extracellular regulated kinase1/2,p-Erk1/2)이급Bcl-2적표체(P＜0.05vsI/R조),이20mg/L적리다잡인억제료SPC대심기Bcl-2표체적상조작용. 결론 20 mg/L적리다잡인취소료SPC적심기보호작용,차효응가능여억제Bcl-2단백표체유관.
Objective To investigate the effects of lidocaine on sevoflurane postconditioning-induced cardioprotection and detect its potential mechanism.Methods Chose healthy adult male Sprague-Dawley rats.Their hearts were excised and perfused in a Langendorff apparatus.After 20 min of equilibration,the hearts subjected to 40 min of ischemia followed by 120 min of reperfusion,then randomly divided into the following seven groups (n=6 each):Sham-operation (Sham),ischemia/reperfusion (I/R),ischemia/reperfusion and 20 mg/L lidocaine(I/R+Lid-20),sevollurane postconditioning(SPC),SPC and 2,10 or 20 mg/L lidocaine (SPC+Lid-2,SPC+Lid-10,SPC+Lid-20).After 20 min of equilibration,the hearts subjected to 40 min of ischemia followed by 120 min of reperfusion.left ventricular developing pressure (LVDP),left ventricular end-diastolic pressure (LVEDP),heart rate (HR),maximal rise/fall rate of left ventricular pressure (±dp/dtmax) and coronary artery flow(CF) were recorded continuously.Coronary effluent was collected at 5 and 10 min of reperfusion for determination of lactate dehydrogenase (LDH) and creatine kinase (CK) activities.Myocardial tissues were obtained at the end of reperfusion for determination of infarct size (IS) and related proteins.Results The LVDP,dp/dtmax,CF were significantly higher and LVEDP,LDH and CK activities,IS [(23.9±1.4)％,(20.5±1.3)％,(24.7±2.1)％vs (47.9±3.3)％] were markedly lower in the SPC,SPC+Lid-2,SPC+Lid-10 groups than in the I/R group at all points of reperfusion (P＜0.05); Compared with group I/R,all the measures were not significantly different in the I/R+Lid-20 and SPC+Lid-20 groups (P＞0.05);The SPC group increased the expression of p-Akt,p-Erk1/2 and Bcl-2,but 20 mg/L lidocaine abolished the increased expression of Bcl-2 induced by SPC.Conclusions 20 mg/L lidocaine inhibits the protective effect induced by SPC and inhibition of Bcl-2 expression may be involved in.
