卡托普利保护大鼠缺血再灌注心肌与抗心肌脂质过氧化的关系(英文)

本实验分别用大鼠在体、离体心脏和培养心肌细胞观察了卡托普利(甲巯丙脯酸)抗心肌缺血再灌注损伤与抗脂质过氧化作用。离体心脏缺氧缺糖45 min后再给氧30 min以及在体心脏缺血3 h后再灌注1h,心肌超氧化物歧化酶(SOD)活性明显下降而丙二醛(MDA)含量显著升高。卡托普利能显著保护再灌注(或再给氧)时心肌SOD活性和降低MDA含量。培养心肌细胞缺氧缺糖6 h,细胞MDA含量和乳酸脱氢酶(LDH)释放显著增加。卡托普利显著降低MDA含量和LDH释放。该作用能被吲哚美辛所取消。IIoprost显示有卡托普利相似的保护作用。结果表明卡托普利的保护作用与抗氧自由基和抗脂质过氧化有关。其机理主要通过促进心肌前列环素释放而发挥作用。

Correlation between cardioprotection of captopril against ischemia/reperfusion damage and myocardial lipid peroxidation in rats

The correlation between the protection of captopril against myocardial ischemia/repcrfusion damage and the inhibition of oxygen free radicals and of lipid pcroxidation was observed in three levels of heart experiments: in vivo,in vitro and in the cultured myocytes of the neonatal rat.In Langcndorff heart after anoxia and glucose-depletion for 45 min followed by 30 min of reoxygcnation,and in intact heart after ischemia for 3 h followed by 1 h rcperfusion,myocardial SOD activity was significantly decreased and MDA content increased.In Langcndorff rat heart,captopril 180μmol/L remarkably preserved SOD activity and reduced MDA content.In rat heart in vivo,the pretreatmcnt captopril 5mg/kg ip at 24 h and 30 min before coronary occlusion also significantly preserved SOD activity.In the cultured myocytes,after anoxia and glucose-depletion for 6 h,both MDA content and LDH release of the myocytes were increased significantly.Captopril 180μmol/L significantly reduced MDA content and LDH release.However,these protections were completely abolished by the pretreatmcnt of indomcthacin.Iloprost,a PGI2 analogue,30nmol/L,showed the similar protective effect of captopril.It is postulated that captopril inhibits oxygen free radicals mainly via the increased release of PGI2 in myocardium,thereby attenuating lipid pcroxidation.