中华麻醉学杂志
中華痳醉學雜誌
중화마취학잡지
CHINESE JOURNAL OF ANESTHESIOLOGY
2009年
5期
453-456
,共4页
邓胜利%喻田%刘兴奎%余志豪
鄧勝利%喻田%劉興奎%餘誌豪
산성리%유전%류흥규%여지호
二氮嗪%线粒体%心脏%再灌注损伤%心磷脂质类
二氮嗪%線粒體%心髒%再灌註損傷%心燐脂質類
이담진%선립체%심장%재관주손상%심린지질류
Diazoxide%Mitochondria,Heart%Reperfusion injury%Cardiolipins
目的 评价线粒体心磷脂在二氮嗪预处理减轻大鼠离体心脏缺血再灌注损伤中的作用.方法 清洁级SD大鼠72只,体重200～280 g,雌雄各半,随机分为对照组(C组)、缺血再灌注组(I/R组)、二氮嗪预处理组(DZ组)和5-羟葵酸拮抗二氮嗪组(HD组),每组18只.采用Langendorff灌流装置建立大鼠离体心脏缺血再灌注模型,C组平衡灌注20 min,持续灌注100 min;I/R组平衡灌注20 min,持续灌注30 min,缺血40 min,再灌注30 min;DZ组平衡灌注20 min后,依次灌注K-H液15 min、50 μmol/L二氮嗪10 min和K-H液5 min,其余缺血再灌注同I/R组;HD组二氮嗪预处理前给予含5-羟葵酸100 μmol/L K-H液10 min,其余处理同DZ组.各组分别于平衡灌注末(T1)、缺血前即刻(T2)、再灌注末(T3)时随机取6只大鼠,监测心率(HR)、左心室发展压(LVDP)和左心室舒张末压(LVEDP),采用高效液相色谱仪测定心肌线粒体心磷脂含量.结果 与T1,2时比较,各组T3时HR、LVDP降低,LVEDP升高,心肌线粒体心磷脂含量降低(P<0.05);与C组比较,其余3组T3时HR、LVDP降低,LVEDP升高,心肌线粒体心磷脂含量降低(P<0.05);与I/R组比较,DZ组T3时HR、LVDP升高,LVEDP降低,心肌线粒体心磷脂含量升高(P<0.05);与DZ组比较,HD组T3时HR、LVDP降低,LVEDP升高,心肌线粒体心磷脂含量降低(P<0.05).结论 二氮嗪预处理可减轻大鼠离体心脏缺血再灌注损伤,与维持心肌线粒体心磷脂含量有关.
目的 評價線粒體心燐脂在二氮嗪預處理減輕大鼠離體心髒缺血再灌註損傷中的作用.方法 清潔級SD大鼠72隻,體重200～280 g,雌雄各半,隨機分為對照組(C組)、缺血再灌註組(I/R組)、二氮嗪預處理組(DZ組)和5-羥葵痠拮抗二氮嗪組(HD組),每組18隻.採用Langendorff灌流裝置建立大鼠離體心髒缺血再灌註模型,C組平衡灌註20 min,持續灌註100 min;I/R組平衡灌註20 min,持續灌註30 min,缺血40 min,再灌註30 min;DZ組平衡灌註20 min後,依次灌註K-H液15 min、50 μmol/L二氮嗪10 min和K-H液5 min,其餘缺血再灌註同I/R組;HD組二氮嗪預處理前給予含5-羥葵痠100 μmol/L K-H液10 min,其餘處理同DZ組.各組分彆于平衡灌註末(T1)、缺血前即刻(T2)、再灌註末(T3)時隨機取6隻大鼠,鑑測心率(HR)、左心室髮展壓(LVDP)和左心室舒張末壓(LVEDP),採用高效液相色譜儀測定心肌線粒體心燐脂含量.結果 與T1,2時比較,各組T3時HR、LVDP降低,LVEDP升高,心肌線粒體心燐脂含量降低(P<0.05);與C組比較,其餘3組T3時HR、LVDP降低,LVEDP升高,心肌線粒體心燐脂含量降低(P<0.05);與I/R組比較,DZ組T3時HR、LVDP升高,LVEDP降低,心肌線粒體心燐脂含量升高(P<0.05);與DZ組比較,HD組T3時HR、LVDP降低,LVEDP升高,心肌線粒體心燐脂含量降低(P<0.05).結論 二氮嗪預處理可減輕大鼠離體心髒缺血再灌註損傷,與維持心肌線粒體心燐脂含量有關.
목적 평개선립체심린지재이담진예처리감경대서리체심장결혈재관주손상중적작용.방법 청길급SD대서72지,체중200～280 g,자웅각반,수궤분위대조조(C조)、결혈재관주조(I/R조)、이담진예처리조(DZ조)화5-간규산길항이담진조(HD조),매조18지.채용Langendorff관류장치건립대서리체심장결혈재관주모형,C조평형관주20 min,지속관주100 min;I/R조평형관주20 min,지속관주30 min,결혈40 min,재관주30 min;DZ조평형관주20 min후,의차관주K-H액15 min、50 μmol/L이담진10 min화K-H액5 min,기여결혈재관주동I/R조;HD조이담진예처리전급여함5-간규산100 μmol/L K-H액10 min,기여처리동DZ조.각조분별우평형관주말(T1)、결혈전즉각(T2)、재관주말(T3)시수궤취6지대서,감측심솔(HR)、좌심실발전압(LVDP)화좌심실서장말압(LVEDP),채용고효액상색보의측정심기선립체심린지함량.결과 여T1,2시비교,각조T3시HR、LVDP강저,LVEDP승고,심기선립체심린지함량강저(P<0.05);여C조비교,기여3조T3시HR、LVDP강저,LVEDP승고,심기선립체심린지함량강저(P<0.05);여I/R조비교,DZ조T3시HR、LVDP승고,LVEDP강저,심기선립체심린지함량승고(P<0.05);여DZ조비교,HD조T3시HR、LVDP강저,LVEDP승고,심기선립체심린지함량강저(P<0.05).결론 이담진예처리가감경대서리체심장결혈재관주손상,여유지심기선립체심린지함량유관.
Objective To investigate the role of mitochondrial cardiolipin in the protective effects of diazoxide preconditioning on isolated rat hearts after ischemia-reperfusion (I/R).Methods Seventy-two healthy SD rats of both sexes (36 male,36 female) weighing 200-280 g were randomly divided into 4 groups ( n = 18 each): group Ⅰ control (group C);group Ⅱ I/R;group Ⅲ diazoxide preconditioning + I/R (group DZ+ I/R) and group Ⅳ 5-hydroxydeconoate (group 5-HD) + DZ + I/R (group 5-HD + DZ + I/R).The animals were anesthetized with intraperitoneal pentobarbital 40 mg/kg.Their hearts were excised and passively perfused in a Langendorff apparatus with oxygenated K-H solution at 5.8 kPa and 37℃.Left ventricular developed pressure (LVDP) was measured from a fluid filled latex balloon inserted in the left ventricle.After 20 min of stabilization the isolated hearts were subjected to 40 min ischemia followed by 30 min reperfusion in group Ⅱ .In group Ⅲ the isolated hearts were perfused with diazoxide 50 μmol/L for 10 min before I/R and in group Ⅳ the isolated hearts were perfused with 5-HD 100 μmol/L for 10 min before diazoxide preconditioning.HR,LVDP and left ventricular end-diastolic pressure (LVEDP) were recorded and mitochondrial cardiolipin content in myecardium was measured at the end of 20 min stabilization (T1,baseline),immediately before ischemia (T2) and at the end of 30 min reperfusion (T3) (6 animals at each time point).Results I/R significantly decreased HR and LVDP and increased LVEDP and decreased mitocbendrial cardiolipin content in myocardium at T3 as compared with the baseline values before ischemia at T1 and T2in group Ⅱ .Diazoxide preconditioning significantly attenuated the I/R induced effects.The protective effects of diazoxide preconditioning against I/R injury was counteracted by 5-HD,a specific mitochondrial ATP sensitive potassium channel blocker.Conclusion Diazoxide preconditioning can protect the myocardium against I/R injury via maintenance of mitochondrial cardiolipin content in myocardium.
