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Chinese Heart Journal. 2003, (06)

Effects of Captopril to reperfusion injury of rat ventricular myocy tes lactate dehydrogenase and malondialdehydeChinese Full Text

CHEN Jian-bin,LI Geng-shan,LI Jian-jun,HUANG Cong-xin,TANG Qi-zhu,WANG Jing (Department of Cardiology,Renmin Hospital,Wuhan University,Wuhan,Hubei 430060,Ch ina)

Abstract: AIM:To observe the effect of Captopril on the injury induced by ano xia-reoxygenation. METHODS:Myocytes were obtained by enzymatic dissoc i ation technique and were divided into 9 groups:normal condition,anoxia,anoxia- r eoxygenation,and 0.05,0.1,0.2,0.4,0.8 and 1.6 μmol/L Captopril reperfusion grou ps. viability of myocytes,lactate dehydrogenase（LDH） activity,LDH activity perce ntage and malondialdehyde（MDA） were measured. RESULTS:There was no cha nge in myocyte viability,LDH releasing activity percentage and MDA in the normal condition group（ P ＞0.05）. In the anoxia group cell viability decreased,and L DH r eleasing activity percentage and MDA increased. And in the anoxia-reoxygenation group,the damage was more serious than that of the anoxia g roup（ P ＜0.01）. There was no statistically significant difference between the anox ia-reoxygenation group and 0.05,0.1 μmol/L Captopril reperfusion groups. C aptop ril inhibited the myocytes contracture,increase the cell viability,reduced forma tion of lipids perxidation products of 0.2,0.4,0.8 and 1.6 μmol/L Captopril rep erfusion groups. And the higher the dose of Captopril,the better the salutar y ef fects. CONCLUSION:Captopril could protect rat ventricular myocytes the anoxia-reoxygenation injury of in a dose-dependent manner,and the myocytes tr ea ted with Captopril were significantly resistant to the anoxia-reoxygenation inju ry.
Keywords：

Captopril; anoxia-reoxygenation injury; myocyte; lact ate dehydrogenase; malondialdehyde;

  • DOI：

    10.13191/j.chj.2003.06.20.chenjb.006

  • Series：

  • Subject：

  • Classification Code：

    R541

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