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N-乙酰半胱氨酸对心衰兔心功能及心肌代谢的影响 被引量:3

Effect of N-Acetylcysteine on Cardiac Function and Myocardial Energy Metabolism of Heart Failure Rabbits
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摘要 目的:探讨N-乙酰半胱氨酸对阿霉素诱导的心衰兔心功能及心肌能量代谢的影响。方法:以阿霉素复制心衰模型,随机分为心衰组和N-乙酰半胱氨酸(NAC)组,药物干预4周,检测各组心衰兔心脏超声学指标、血流动力学指标、心肌病理形态学改变以及血清和心肌组织游离脂肪酸(FFA)、乳酸(LD)含量和ATP酶活力的变化,观察NAC对上述指标的影响。结果:心衰组兔左室舒张期末内径、左室收缩期末内径增大,有显著性差异(P<0.05);射血分数与短轴缩短率降低,有显著性意义(P<0.05),NAC干预组各指标较心衰组明显改善。心衰组心功能指标比对照组明显下降(P<0.01),NAC干预组心功能指标好转(P<0.05)。心衰组兔心肌组织可见明显病理性改变,而经NAC治疗4周后无明显病理性改变。心衰组血清和心肌FFA、LD含量均明显高于对照组,ATP酶(钠-钾ATP酶、钙ATP酶)活力降低,NAC治疗4周以后FFA、LD明显下降,ATP酶活力高于心衰组。结论:NAC可以改善心衰兔心肌细胞的能量代谢,改善其心肌能量缺乏和收缩能力,从而改善心功能。 Objective:To investigate the effect of N-acetylcysteine(NAC)on cardiac function and myocardium energy metabolism of heart failure rabbits.Methods:An animal model of heart failure was induced by adriamycin(ADR)in rabbits.The animals were randomly assigned into two groups:heart failure group and N-acetylcysteine group.After four weeks of treatment,heart ultrasonic parameters,hemodynamic parameters,the level of FFA and LD,and ATPase activity in blood and myocardium were determined,then the effects of NAC on the above indexes were also observed.Results:In the heart failure group,LVEDD and LVDSD were significantly higher than those of control group(P〈0.05),while EF,FS,and hemodynamic parameters were significantly lower than those of control group(P〈0.01).NAC can improve heart ultrasonic and hemodynamic parameters in rabbits with heart failure(P〈0.05).There were obviously pathological changes in myocardial tissue of heart failure group,but the NAC treated group showed no obvious pathological changes in the myocardial tissue.In the heart failure group,the FFA and LD levels were significantly higher than those of control group(P〈0.05),while ATPase activity(Na+-K+ATPase and Ca2+ATPase)was significantly lower(P〈0.05).NAC can reduce FFAand LD level and improve ATPase activity(Na+-K+ATPase and Ca2+ATPase)in rabbits with heart failure(P〈0.05).Conclusion:NAC can improve myocardial cell energy metabolism of heart failure rabbit,relieve its energy deficiency,and enhance its contraction ability,then improve its heart function.
出处 《武汉大学学报(医学版)》 CAS 北大核心 2014年第5期678-682,688,共6页 Medical Journal of Wuhan University
基金 湖北省自然科学基金资助项目(编号:2013CFB248)
关键词 心力衰竭 N-乙酰半胱氨酸 心肌能量代谢 Heart Failure N-Acetylcysteine Myocardium Energy Metabolism
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  • 1WANG Jun1,2, BAI Ling1,2, LI Jing3, SUN ChaoFeng1,2, ZHAO Jin1, CUI ChangCong1,2, HAN Ke1,2, LIU Yu1,2, ZHUO XiaoZhen1,2, WANG TingZhong1,2, LIU Ping1,2, FAN FenLing1,2, GUAN YouFei3 & MA AiQun1,2 1 Department of Cardiology, First affiliated hospital of medical college of Xi’an Jiaotong University, Xi’an 710061, China,2 Ion Channel Disease Laboratory, Key Laboratory of Environment and Genes Related to Diseases of Education Ministry, Xi’an 710061, China,3 Department of Physiology and Pathophysiology,Key Laboratory of Molecular Cardiovascular Sciences of the Ministry of Education, Peking University Health Science Center, Beijing 100083, China.Proteomic analysis of mitochondria reveals a metabolic switch from fatty acid oxidation to glycolysis in the failing heart[J].Science China(Life Sciences),2009,52(11):1003-1010. 被引量:11

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