重庆医学
重慶醫學
중경의학
CHONGQING MEDICAL JOURNAL
2014年
27期
3596-3598
,共3页
心肌梗死%辛伐他汀%氧化应激%心室重塑
心肌梗死%辛伐他汀%氧化應激%心室重塑
심기경사%신벌타정%양화응격%심실중소
myocardial infarction%simvastatin%oxidative stress%ventricular remodeling
目的:建立大鼠心肌梗死的模型,观察不同剂量辛伐他汀抑制心肌梗死后氧化应激的作用,探讨不同剂量辛伐他汀改善大鼠心室重塑和心功能的潜在机制。方法结扎大鼠冠状动脉前降支,形成急性心肌梗死模型,给予不同剂量辛伐他汀(20、40、60 mg · kg -1· d-1)干预。4周后,测定心脏心室重塑的各项指标,检测不同分组的大鼠心肌中总超氧化物歧化酶(SOD )、铜锌-超氧化物歧化酶(CuZn-SOD)活性、血液H2 O2水平,并与假手术组比较。结果心肌梗死组大鼠心室重塑明显,左室心脏重量指数(LVWI)升高,心率增快,血流动力学紊乱(P<0.05)。心肌中SOD、CuZn-SOD和血液中 H2O2水平升高(P<0.05)。不同剂量辛伐他汀干预组均较心肌梗死组LVWI下降(P<0.05),心肌中SOD、CuZn-SOD和血液中 H2 O2水平下降,心率减慢,血流动力学改善(P<0.05),尤其以高剂量他汀干预组(60 mg · kg -1· d-1)更明显。结论辛伐他汀减少急性心肌梗死后氧化应激表达,可能是改善心室重塑和心功能的机制之一,并与剂量有一定的正相关性。
目的:建立大鼠心肌梗死的模型,觀察不同劑量辛伐他汀抑製心肌梗死後氧化應激的作用,探討不同劑量辛伐他汀改善大鼠心室重塑和心功能的潛在機製。方法結扎大鼠冠狀動脈前降支,形成急性心肌梗死模型,給予不同劑量辛伐他汀(20、40、60 mg · kg -1· d-1)榦預。4週後,測定心髒心室重塑的各項指標,檢測不同分組的大鼠心肌中總超氧化物歧化酶(SOD )、銅鋅-超氧化物歧化酶(CuZn-SOD)活性、血液H2 O2水平,併與假手術組比較。結果心肌梗死組大鼠心室重塑明顯,左室心髒重量指數(LVWI)升高,心率增快,血流動力學紊亂(P<0.05)。心肌中SOD、CuZn-SOD和血液中 H2O2水平升高(P<0.05)。不同劑量辛伐他汀榦預組均較心肌梗死組LVWI下降(P<0.05),心肌中SOD、CuZn-SOD和血液中 H2 O2水平下降,心率減慢,血流動力學改善(P<0.05),尤其以高劑量他汀榦預組(60 mg · kg -1· d-1)更明顯。結論辛伐他汀減少急性心肌梗死後氧化應激錶達,可能是改善心室重塑和心功能的機製之一,併與劑量有一定的正相關性。
목적:건립대서심기경사적모형,관찰불동제량신벌타정억제심기경사후양화응격적작용,탐토불동제량신벌타정개선대서심실중소화심공능적잠재궤제。방법결찰대서관상동맥전강지,형성급성심기경사모형,급여불동제량신벌타정(20、40、60 mg · kg -1· d-1)간예。4주후,측정심장심실중소적각항지표,검측불동분조적대서심기중총초양화물기화매(SOD )、동자-초양화물기화매(CuZn-SOD)활성、혈액H2 O2수평,병여가수술조비교。결과심기경사조대서심실중소명현,좌실심장중량지수(LVWI)승고,심솔증쾌,혈류동역학문란(P<0.05)。심기중SOD、CuZn-SOD화혈액중 H2O2수평승고(P<0.05)。불동제량신벌타정간예조균교심기경사조LVWI하강(P<0.05),심기중SOD、CuZn-SOD화혈액중 H2 O2수평하강,심솔감만,혈류동역학개선(P<0.05),우기이고제량타정간예조(60 mg · kg -1· d-1)경명현。결론신벌타정감소급성심기경사후양화응격표체,가능시개선심실중소화심공능적궤제지일,병여제량유일정적정상관성。
Objective To establish the rat myocardial infarction model to observe the effects of different kinds of doses of simv-astatin for inhibiting the oxidative stress after myocardial infarction ,and to explore the potential mechanism of different doses of simvastatin for improving the rat ventricular remodeling and cardiac function .Methods The coronary artery anterior descending branch was ligated for establishing the myocardial infarction rat model and the different doses of simvastatin (20 ,40 ,60 mg · kg -1 · d-1 ) were given for intervention .After 4 weeks ,the cardiac ventricular remodeling indicators ,superoxide dismutase(SOD) and cop-per zinc superoxide dismutase(CuZn-SOD) activity in myocardium ,blood H2 O2 level were detected and the detection results were compared with those in the sham operation group .Results The rat ventricular remodeling in the myocardial infarction group (M group) was significant ,the left ventricular mass index (LVWI) was elevated ,the heart rate was increased and the hemodynamics was disordered(P<0 .05) .The SOD and CuZn-SOD expression in the myocardium and blood H2O2 expression were elevated(P<0 .05) .The LVW1 in different doses of simvastatin intervention groups were decreased compared with the myocardial infarction group(P<0 .05) ,the heart rate was decreased ,SOD and CuZn-SOD expression and blood H2 O2 expression were decreased ,the he-modynamics was improved(P<0 .05) ,especially which in the high dose atorvastatin intervention group (60 mg · kg -1 · d-1 ) were more significant .Conclusion Simvastatin reduces the expression of oxidative stress after acute myocardial infarction ,which may be one of the mechanisms for improving the ventricular remodeling and heart function ,and has certain positive correlation with dose .