血管紧张素转换酶抑制剂对缺氧心肌细胞的保护机制  

Protective Effects of Angiotensin Converting Enzyme Inhibitors on Cultured Rat Cardiac Myocytes Injured by Anoxia

作　　者：张建青[1] 刘伊丽[1] 赖世忠[1] 刘俭[1] 

机构地区：[1]中国人民解放军第一军医大学附属南方医院

出　　处：《中国循环杂志》1996年第10期595-598,共4页Chinese Circulation Journal

摘　　要：目的：探讨血管紧张素转换酶抑制剂对缺氧心肌细胞的保护机制。方法：培养Ｗｉｓｔａｒ大鼠心肌细胞，７２小时后分为对照组、卡托普利组、依那普利拉组、缺氧组、缺氧加卡托普利组、缺氧加依那普利拉组。药物终浓度为１０－５ｍｏｌ／Ｌ。前３组采用有氧培养，后３组应用低糖无氧培养３０分钟。在ＭＰＶ３型显微分光光度计下测定心肌细胞内乳酸脱氢酶、琥珀酸脱氢酶相对含量，并取细胞上清液应用生化分析仪测定细胞内酶漏出情况。实验结果采用ｔ检验。结果：卡托普利和依那普利拉均可提高心肌细胞内乳酸脱氢酶含量（与对照组、缺氧组相比Ｐ＜０．０１）；减少缺氧心肌细胞内酶的漏出（与缺氧组相比Ｐ＜０．０１）。结论：血管紧张素转换酶抑制剂可明显改善缺氧心肌细胞糖代谢，加速糖酵解，减轻缺氧性损伤，对缺氧心肌细胞具有一定的保护作用。Objective:To observe the protective mechanism of captopril(cap) and enalaprilat(ena) on anoxic cardiac myocytes. Methods:Rat cardiac myocytes were cultured and divided into six groups(control,cap,ena,anoxia,anoxia+cap and anoxia+ena)after 72 hours.Drug concentration was 10 5 mol/L.Anoxia was produced with depletion of oxygen and metabolic substrates for 30 min.The relative contents of lactic dehydrogenase(LDH)and succinic dehydrogenase (SDH) of cardiac myocytes were measured with microspectrophotometer and the activities of aspartate aminotransferase (AST) ,lactic dehydrogenase (LDH) and creatine kinase(CK) in the culture media were measured with automatic analyzer.Statistical analysis was performed by Student′s test. Results:Both captopril and enalaprilat increased the activity of LDH within the control and anoxic cardiac myocytes( p <0 01) and decreased AST, LDH and CK activities in the culture media( p <0 01 vs.anoxia group). Conclusion:Both captopril and enalaprilat could improve glucose metabolism of anoxic cardiac myocytes.This may play a special role in the maintenance of membrane integrity and function of anoxiadamaged cardiac myocytes in culture.

关 键 词：血管紧张素 转换酶 抑制剂 心肌缺氧 

分 类 号：R541.405[医药卫生—心血管疾病]