辛伐他汀对自由基引起的离体大鼠心肌损伤的保护作用  

Simvastatin induced myocardial protection against free radical inyury in rat isolated heart

作　　者：钟蓓华[1] 罗健东[1] 张贵平[1] 区慧坚[1] 

机构地区：[1]广州医学院药理学教研室,广州510182

出　　处：《中国药理学通报》2000年第6期651-654,共4页Chinese Pharmacological Bulletin

摘　　要：目的　探讨在大鼠离体灌流心脏预先给予辛伐他汀能否对抗自由基引起的心肌功能损伤。方法　在Langen dorff离体大鼠心脏上观察辛伐他汀能否拮抗DPPH自由基对离体心功能的损伤 ,记录左心室收缩功能指标 ,冠脉流量(CF) ,心率 (HR)及心肌组织脂质过氧化物丙二醛 (MDA)的生成。结果　在DPPH自由基损伤对照组LVDP ,+dp/dtmax,CF ,HR较正常对照组下降 (P <0 0 1) ,而MDA的生成较正常对照组升高 (P <0 0 1)。预先给予含辛伐他汀的灌流液灌流 15min ,再用含DPPH自由基的灌流液灌流心脏 ,结果显示心脏收缩功能指标LVDP ,+dp/dtmax较DPPH自由基损伤组改善 (P <0 0 1) ,而MDA的生成较DPPH自由基损伤对照组减少 (P <0 0 1)。CF及HR较DPPH损伤组也稍有改善。结论　辛伐他汀对DPPH自由基引起的心肌损伤具有明显的保护作用。AIM To examine whether pretreatment with simvastatin protects the heart against free radical injury. METHODS 1 1 diphenyl 2 picryl hydrazyl (DPPH) was used for triggering free radical injury in cardiac tissue. Simvastatin against free radical injury was investigated in a Langendorff fused rat heart. Left ventricular developed pressure (LVDP), maximal velocity of increase of LVP (+d p /d t max ), heart rate (HR) coronary flow (CF) and malondialdehyde (MDA) formation in cardiac tissue were measured. RESULT In the DPPH free radical group, DPPH signficantly decreased LVDP, +d p /d t max , HR was slowed and CF was reduced. The formation of MDA was significantly enhanced. ( P <0 01 vs control). Simvastatin perfusion for 15 min protected the heart against DPPH free radical induced functional impairment, with significant improvement in LVDP, +d p /d t max , HR and CF. The formation of MDA was reduced. In conclusion, pretreatment with simvastatin results in cardiac protection against free radical injury.

关 键 词：辛伐他汀 自由基 丙二醛 心肌保护作用 心肌损伤 

分 类 号：R972[医药卫生—药品] R542.2[医药卫生—药学]