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贾钰华,余林中,陈育尧,周轶林,孙学刚.定心方对家兔心肌缺血及再灌注损伤的保护作用和抗心律失常作用的研究[J].中国中西医结合杂志,1999,(11):678-681
定心方对家兔心肌缺血及再灌注损伤的保护作用和抗心律失常作用的研究
Effect of Dingxin Recipe on Arrhythmia and Injury Induced by Ischemia and Reperfusion in Rabbits
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DOI:
中文关键词:  定心方  心肌缺血  再灌注  心律失常
英文关键词:Dingxin Recipe  myocardial ischemia  reperfusion  arrhythmia
基金项目:国家中医药管理局科研基金!No .95B1 54
作者单位
贾钰华 第一军医大学中医系!广州510515 
余林中 第一军医大学中医系!广州510515 
陈育尧 第一军医大学中医系!广州510515 
周轶林 第一军医大学中医系!广州510515 
孙学刚 第一军医大学中医系!广州510515 
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中文摘要:
      目的:研究定心方(DXR)抗兔心肌缺血及再灌注损伤和抗心律失常作用。方法:兔冠状动脉双重结扎造成心肌梗塞,观察各组心律失常情况并检测血浆超氧化物歧化酶(SOD)、cAMP、去甲肾上腺素(NE)、多巴胺(DA)、5羟色胺(5HT),观察心肌超微结构。结果:DXR对兔心肌梗塞后心律失常有拮抗作用,其中DXR大剂量组与对照组比较有显著性差异(P<001);对缺血再灌注心律失常也有拮抗作用,DXR大、小剂量组与对照组比较均有显著性差异(P<001);对上述状态的心电图ST-T抬高有改善作用。实验表明,DXR能升高血清SOD浓度,而使cAMP、NE、DA、5HT浓度和全血粘度降低。结论:DXR能拮抗心肌缺血及再灌注损伤和心律失常,其机理可能通过清除氧自由基、调节细胞第二信使、抑制交感神经系统、改善局部循环,保护线粒体、抑制溶酶体活化使心肌细胞免受损伤而实现。
英文摘要:
      To investigate the protective effect of Dingxin Recipe (DXR) on arrhythmia and injury induced by ischemia and reperfusion. Methods: Rabbits were randomly divided into four groups and administered orally with DXR of high dose, low dose, propanolol and distilled water. Two step coronary artery ligature was used to form ischemia and reperfusion model. Superoxide dismutase (SOD), cyclic adenosine monophosphate (cAMP), norepinephrine (NE), dopamine (DA), 5 hydroxytryptamine (5 HT), myocyte ultrastructural injury and occurrence of arrhythmia were investigated. Results: DXR could obviously antagonize arrhythmia induced by myocardial infarction or ischemia and reperfusion in rabbits. Compared with the control group, DXR of high and low doses could improve the changes in ST T. In rabbits treated with DXR, the levels of SOD were elevated while cAMP, NE, DA, 5 HT and the whole blood viscosity were lowered. Conclusions: DXR could obviously antagonize arrhythmia and injury induced by ischemia and reperfusion, DXR may clear oxygen free radical, regulate the second messenger, inhibit sympathetic nerve system, improve local circulation, protect mitochondria and prevent the activation of lysosome and safeguard the cardiac myocyte to be free from injury.
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