医学临床研究
醫學臨床研究
의학림상연구
JOURNAL OF CLINICAL RESEARCH
2013年
8期
1475-1477
,共3页
樊纯铁%冉珂%李志坚%常业恬
樊純鐵%冉珂%李誌堅%常業恬
번순철%염가%리지견%상업념
再灌注损伤%心肌缺血%硫化氢%S-腺苷甲硫氨酸%大鼠
再灌註損傷%心肌缺血%硫化氫%S-腺苷甲硫氨痠%大鼠
재관주손상%심기결혈%류화경%S-선감갑류안산%대서
Reperfusion Injury%Myocardial Ischemia%Hydrogen Sulfide%S-Adenosylmethionine%Rats
[目的]探讨硫化氢(H2 S)预处理对大鼠心肌缺血再灌注时S-腺苷蛋氨酸合成酶( SAM-s)表达的影响。[方法]健康成年S-D雄性大鼠50只,随机分成5组,每组10只。假手术组(S组)仅开胸并分离冠状动脉左前降支,但不阻断血流150 min;缺血再灌注组(IR组)行冠状动脉左前降支阻断30 min ,再灌注120 min;硫化氢1组(H1组)予以静脉注射硫氢化钠(NaHS)0.025 mg/kg ,给药后24 h同IR组处理;H2 S2组(H2组)予以静脉注射NaHS 0.05 mg/kg ,给药后24 h同IR组处理;H2 S3组(H3组)予以静脉注射NaHS 0.10 mg/kg ,给药后24 h同IR组处理。再灌注结束后测心肌梗死面积,免疫印迹法测心肌SAM-s的表达。[结果]与IR组心肌梗死面积(38.27%±5.64%)比,各H2 S组心肌梗死面积均减小( P <0.05)。与S组比,IR组和 H2 S组SAM-s均升高( P <0.05),与IR组比,各H2 S组SAM-s表达均降低( P <0.05)。[结论]H2 S预处理对大鼠心肌损伤的保护作用可能与其抑制心肌SAM-s表达有关。
[目的]探討硫化氫(H2 S)預處理對大鼠心肌缺血再灌註時S-腺苷蛋氨痠閤成酶( SAM-s)錶達的影響。[方法]健康成年S-D雄性大鼠50隻,隨機分成5組,每組10隻。假手術組(S組)僅開胸併分離冠狀動脈左前降支,但不阻斷血流150 min;缺血再灌註組(IR組)行冠狀動脈左前降支阻斷30 min ,再灌註120 min;硫化氫1組(H1組)予以靜脈註射硫氫化鈉(NaHS)0.025 mg/kg ,給藥後24 h同IR組處理;H2 S2組(H2組)予以靜脈註射NaHS 0.05 mg/kg ,給藥後24 h同IR組處理;H2 S3組(H3組)予以靜脈註射NaHS 0.10 mg/kg ,給藥後24 h同IR組處理。再灌註結束後測心肌梗死麵積,免疫印跡法測心肌SAM-s的錶達。[結果]與IR組心肌梗死麵積(38.27%±5.64%)比,各H2 S組心肌梗死麵積均減小( P <0.05)。與S組比,IR組和 H2 S組SAM-s均升高( P <0.05),與IR組比,各H2 S組SAM-s錶達均降低( P <0.05)。[結論]H2 S預處理對大鼠心肌損傷的保護作用可能與其抑製心肌SAM-s錶達有關。
[목적]탐토류화경(H2 S)예처리대대서심기결혈재관주시S-선감단안산합성매( SAM-s)표체적영향。[방법]건강성년S-D웅성대서50지,수궤분성5조,매조10지。가수술조(S조)부개흉병분리관상동맥좌전강지,단불조단혈류150 min;결혈재관주조(IR조)행관상동맥좌전강지조단30 min ,재관주120 min;류화경1조(H1조)여이정맥주사류경화납(NaHS)0.025 mg/kg ,급약후24 h동IR조처리;H2 S2조(H2조)여이정맥주사NaHS 0.05 mg/kg ,급약후24 h동IR조처리;H2 S3조(H3조)여이정맥주사NaHS 0.10 mg/kg ,급약후24 h동IR조처리。재관주결속후측심기경사면적,면역인적법측심기SAM-s적표체。[결과]여IR조심기경사면적(38.27%±5.64%)비,각H2 S조심기경사면적균감소( P <0.05)。여S조비,IR조화 H2 S조SAM-s균승고( P <0.05),여IR조비,각H2 S조SAM-s표체균강저( P <0.05)。[결론]H2 S예처리대대서심기손상적보호작용가능여기억제심기SAM-s표체유관。
[Objective] To explore the effect of hydrogen sulfide preconditioning on the expression of S-adeno-sylmethionine synthetase during myocardial ischemia reperfusion in rats .[Methods] Totally 50 healthy SD male rats were randomly divided into 5 groups with 10 in each .Sham operation group(group S) underwent thoracotomy with separating left anterior descending coronary artery but without blocking blood flow for 150min .Ischemia reperfusion group(group IR) was given intravenous injection with NaHS 0 .025mg/kg ,and then the same treat-ment of IR group 24h later .Hydrogen sulfide 2 group(group H2) was given intravenous injection with NaHS 0 . 05mg/kg ,and then the same treatment of IR group IR 24h later .Hydrogen sulfide 3 group(group H3) was given intravenous injection with NaHS 0 .10mg/kg ,and then the same treatment of IR group 24h later .At the end of reperfusion ,myocardial infarct size was measured ,and the expression of SAM-s was detected by Western blot-ting .[Results] Compared with myocardial infarct size of IR group (38 .27 % ± 5 .64 % ) ,myocardial infarct size in other hydrogen sulfide groups was decreased ( P <0 .05) .Compared with group S ,the expression of SAM-s in group IR and group H was increased( P<0 .05) .Compared with group IR ,the expression of SAM-s in other hy-drogen sulfide groups was decreased( P <0 .05) .[Conclusion]Hydrogen sulfide preconditioning attenuates myo-cardial ischemia reperfusion injury possibly through down-regulating SAM-s expression in rats .