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曲美他嗪对家兔心肌缺血再灌注损伤的保护作用
引用本文:王健,黄元伟,魏经汉,魏太星,董建增,张金盈.曲美他嗪对家兔心肌缺血再灌注损伤的保护作用[J].浙江大学学报(医学版),2003,32(3):219-222.
作者姓名:王健  黄元伟  魏经汉  魏太星  董建增  张金盈
作者单位:1. 浙江大学医学院附属第一医院,浙江,杭州,310003
2. 郑州大学附属第一医院,河南,郑州,450052
摘    要:目的 :探讨曲美他嗪对家兔心肌缺血再灌注损伤的保护作用。方法 :家兔 4 0只 ,随机分为正常对照组、缺血对照组、缺血药物干预组、再灌注对照组、再灌注药物干预组。观察缺血 30 min和再灌注 30 min对血清肌酸磷酸激酶 (CPK)、丙二醛 (MDA)、超氧化物歧化酶 (SOD)的影响 ,心肌三磷酸腺苷 (ATP)含量 ,以及心肌电镜学改变。结果 :1缺血药物干预组与缺血对照组比较 ,除血清 MDA差异有显著性外 (4 .0 9± 0 .4 0 vs4 .79± 0 .92 ) nmol/ ml,P<0 .0 1],血清 CPK(132 2± 114 8vs14 98± 190 ) NU/ ml]、SOD(32 4± 71vs2 88± 5 4) NU/ ml]差异均无显著性(P>0 .0 5 )。 2再灌注药物干预组与再灌注对照组比较 ,血清 CPK(15 12± 2 2 6 vs190 4± 2 0 3) NU/ ml]、MDA(6 .0 9± 0 .6 9vs7.4 3± 0 .2 0 ) nmol/ ml]、SOD(2 13± 71vs119± 5 5 ) NU/ ml],及缺血区心肌 ATP含量 (1.4 0 1± 0 .2 4 8vs0 .6 2 9± 0 .175 ) μmol/ g]差异均有显著性 (P<0 .0 0 1~ 0 .0 1)。 3电镜显示 :各药物干预组线粒体结构改变分别较各对照组减轻。结论 :曲美他嗪具有改善缺血再灌注损伤心肌线粒体的代谢和清除氧自由基的功能。

关 键 词:心肌缺血  再灌注损伤  曲美他嗪  家兔  保护作用
文章编号:1008-9292(2003)03-0219-04
修稿时间:2001年12月17

Protective effect of trimetazidine on rabbit myocardium during ischemia-reperfusion
WANG Jian,HUANG Yuan-wei,WEI Jing-han,et al.Protective effect of trimetazidine on rabbit myocardium during ischemia-reperfusion[J].Journal of Zhejiang University(Medical Sciences),2003,32(3):219-222.
Authors:WANG Jian  HUANG Yuan-wei  WEI Jing-han  
Institution:The First Affiliated Hospital, College of Medical Sciences, Zhejiang University, Hangzhou 310003, China.
Abstract:OBJECTIVE: To investigate the protective effects of trimetazidine on rabbit myocardium in ischemia and reperfusion. METHODS: Fourty rabbits were divided into five groups randomly: normal control group, ischemia control group, ischemia and drug intervention group, reperfusion control group, reperfusion and drug intervention group. Ischemia lasted for 30 minutes and reperfusion was given for 30 minutes. Serum CPK, SOD activities and MDA concentrations were measured in each group and ischemia tissue ATP concentrations were also measured. Heart tissue was examined with electron microscope in each group. RESULTS: (1) Serum concentrations of MDA in ischemia and drug intervention group were significantly different from those in ischemia control group (4.09+/-0.40 vs 4.79+/-0.92)nmol/ml, P<0.01], serum activities of CPK (1322+/-1148 vs 1498+/-190) NU/ml], SOD(324+/-71 vs 288+/-54)NU/ml] were not significantly different between ischemia and drug intervene group and ischemic control group (PP>0.05,respectively). (2) Serum activities of CPK (1512+/-226 vs 1904+/-203) NU/ml], SOD(213+/-71 vs 119+/-55) NU/ml], concentrations of MDA (6.09+/-0.69 vs 7.43+/-0.20)nmol/ml] and concentrations of ATP(1.401+/-0.248 vs 0.629+/-0.175) micromol/g] in ischemia heart tissue of reperfusion and drug intervention group were significantly different from those in reperfusion control group (P<0.001 - 0.01 respectively). (3) There were significant differences in electron microscopic observation between intervention group and control group. CONCLUSION: Trimetazidine can improve cardiac mitochondrial metabolism and scavenge oxygen free radicals. Trimetazidine has cardioprotective function during ischemia and reperfusion.
Keywords:Trimetazidine/pharmacol  Myocardial ischemia  Reperfusion injury/drug eff  Creatine kinase/blood  Superoxide dismutase/blood  Adenosine triphate  Rabbit  
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