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辅酶NADH对大鼠心肌缺血再灌注损伤生化标志物含量的影响
引用本文:马海峰,张培喜,郑建伟,于文舟.辅酶NADH对大鼠心肌缺血再灌注损伤生化标志物含量的影响[J].潍坊医学院学报,2009,31(1):29-32.
作者姓名:马海峰  张培喜  郑建伟  于文舟
作者单位:1. 潍坊医学院外科学教研室,山东,潍坊,261042
2. 济宁市第一人民医院心胸外科
3. 潍坊市人民医院心外科
摘    要:目的观察还原型烟酰胺腺嘌呤二核苷酸(NADH)对大鼠心肌缺血再灌注损伤的保护作用。探讨其可能的保护机制。方法选取健康雄性Wistar大鼠制备心肌缺血再灌注模型,雄性Wistar大鼠80只,随机分为4组,每组20只,分别为:缺血再灌注(MIR)模型组,NADH低剂量组(5mg/kg),NADH中剂量组(10mg/kg),NADH高剂量组(15mg/kg)。缺血再灌注(MIR)组:左前降支结扎前30min,5%葡萄糖腹腔注射;NADH低、中、高剂量组于结扎前30min,分别给予NADH5mg/kg、10mg/kg、15mg/kg腹腔注射。以上各组造模成功者分别随机分为:缺血30min和再灌注60min两组。观察大鼠血液中乳酸脱氢酶(1actate dehydrogenase,LDH)、肌酸激酶同工酶(MB isoenzyme of creatine kinase,CK-MB)、丙二醛(malondialdehyde,MDA)、羟自由基、总超氧化物歧化酶(total superoxide dismutase,T—SOD)含量的变化。结果与缺血再灌注(MIR)组比较,各处理组再灌后MDA、羟自由基、LDH、CK—MB释放水平明显降低,而T—SOD的水平升高,有统计学意义。结论NADH能够减少缺血再灌注引发的心肌细胞的一系列损伤,对心肌缺血再灌注损伤有保护作用,且达到治疗量(5mg/kg)后这种保护作用不具有剂量依赖性。

关 键 词:再灌注损伤  还原型烟酰胺腺嘌呤二核苷酸  羟自由基  心肌型肌酸激酶同工酶

The Effect of Coenzyme NADH on Biochemical Markers of Myocardial Ischemia Reperfusion Injury in Rats
MA Hai-feng,ZHANG Pei-xi,ZHENG Jian-wei,YU Wen-zhou.The Effect of Coenzyme NADH on Biochemical Markers of Myocardial Ischemia Reperfusion Injury in Rats[J].Journal of Weifang Medical College,2009,31(1):29-32.
Authors:MA Hai-feng  ZHANG Pei-xi  ZHENG Jian-wei  YU Wen-zhou
Institution:MA Hai-feng ,ZHANG Pei-xi ,ZHENG Jian-wei , YU Wen-zhou (1 Department of Surgery, Weifang Medical College, Weifang 261042, China ; 2 Department of Cardio-Thoracic Surgery, JiNing First People's Hospital ;3 Department of Cardiacsurgery, Weifang People's Hospital)
Abstract:Objective To investigate the effect of NADH during myocardial ischemia reperfusion injury in rats and approach its protective mechanism. Methods Eighty male Wistar rats were divided into four groups randomly:①Myocardial ischemia reperfusion injury (MIR) group;②NADH 5mg/kg treated group;③NADH 10mg/kg treated group;④NADH 15mg/kg treated group. Male Wistar rats were anesthetized and the left coronary artery was ligated for 30 minutes and then reperfused for 60 minutes, studying the effect of NADH ( reduced form of nicotinamide-adenine dinucleotid ) on change of MDA ( malondialdehyde ) , hydroxy radical, LDH ( lactate dehydrogenase ) , CK-MB ( MB isoenzyme of creatine kinase) and SOD ( superoxide dismutase ) during myocardial ischemia reperfusion injury in rats. Two rats died of ventricular fibrillation in the MIR group. Two rats died of ventricular fibrillation in the NADH 5mg/kg treated group. One rat died of ventricular fibrillation in the N ADH 15mg/kg treated group. Results Compared with MIR group,the release level of MDA, CK-MB, LDH, and hydroxy radical significantly decreased while that of SOD increased after reperfusion in the other group. Conclusion NADH can prevent myocardium from ischemia reperfusion injury in experimental ischemia reperfusion rats. And this effect is not in a dose-dependent manner.
Keywords:Myocardial reperfusion injury  Reduced form of nicotinamide-adenine dinucleotid  Hydroxy radical  Isoenzyme of creatine kinase
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