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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。
Objective To investigate whether pre-administration of simvastatin in rat perfused heart can antagonize free radical-induced myocardial dysfunction. Methods To observe whether simvastatin could antagonize the injury of isolated DPPH free radical in isolated rat hearts and to record left ventricular systolic function, coronary flow (CF), heart rate (HR) and myocardial tissue lipids Production of malondialdehyde (MDA). Results Compared with normal control group, LVDP, dp / dtmax, CF and HR in DPPH-induced group were lower than those in normal control group (P <0.01), while MDA level was higher than that in control group (P <0.01). Perfusion of simvastatin-containing perfusate for 15 min followed by perfusion of the heart with DPPH-free perfusate showed that LVDP and dp / dtmax were significantly improved (P <0.01) , While the MDA production was lower than that of DPPH free radical injury control group (P <0.01). CF and HR also slightly improved compared with DPPH lesion group. Conclusion Simvastatin has a significant protective effect on myocardial injury induced by DPPH free radicals.