辛伐他汀抑制急性心肌梗死后心肌氧化损伤的实验研究

目的观察辛伐他汀抑制急性心肌梗死后心肌氧化损伤的作用,并探讨其可能的机制.方法结扎大鼠冠状动脉前降支造成心肌梗死模型,给予辛伐他汀干预. 8周后,测定血流动力学指标、心肌及血液中总超氧化物歧化酶(SOD)、铜锌-超氧化物歧化酶(CuZn-SOD)活性;血液过氧化氢(H2O2)含量,并与假手术组比较. 结果心肌梗死组(M组)大鼠外周动脉压(APS)、舒张压(APD)均降低,心率增快(P<0.01).LVSP和 dp/dtmax,-dp/dtmax下降(P<0.01), LVEDP升高(P<0.01);心肌、血液中SOD及CuZn-SOD活性下降,H2O2含量升高(P<0.01).辛伐他汀干预组较M组APS、APD、LVSP、 dp/dtmax、-dp/dtmax均回升(P<0.01),LVEDP回落(P<0.01);血清和心肌SOD及CuZn-SOD活性升高,H2O2含量下降.结论辛伐他汀改善急性心肌梗死后心功能,可能与其提高SOD活性抗氧化损伤有关.

Experimental study of abating oxidative damage after acute myocardium infarction by Simvastatin

Objective To investigate the effects of Simvastatin abating oxidative damage after myocardium infarction and the possible mechanisms.Methods Simvastatin was given to the rats with myocardiac infarction by left anterior decending coronaryartery ligation.After 8 weeks,changes of hemodynamics were observed.The activity of superoxide dismutase(SOD) and copper-zinc SOD (CuZu-SOD) in left ventdcular and hydrogen peroxide(H 2O 2) in serum were measured.Results In the rat model of myocardiac infarction,left ventricular systolic pressure(LVSP), the ventricular pressure dse ratio during systolic period( dp/dt max ),the ventricular pressure rise decay ratio during diastolic period(-dp/dt max )decline(eachP<0.01)and left ventricular end diastolic pressure(LVEDP)rise(P<0.01).The activity of SOD CuZu-SOD in left ventricular decrease and H 2O 2 in serum increase.Simvastatin enhance LVSP, dp/dt max ,-dp/dt max (each P<0.01)and decline LVEDP(P<0.01).SOD CuZu-SOD activity increase and content of H 2O 2 in serumdecrease(each P<0.01).Conclusion Ameliorating the condition of hemodynamics in Simvastatin attenuated oxidative damage after myocardiac infraction may be one of the mechanisms.