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葡萄糖酸镁对大鼠心肌缺血再灌注损伤的保护作用

Cardioprotective Effects of Magnesium Gluconateon on Myocardial Ischemia Reperfusion Injury in Rats
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摘要 目的 观察葡萄糖酸镁对心肌缺血 -再灌注损伤过程中血清NO浓度、组织内丙二醛 (MDA)及Ca2 +浓度的影响 ,探讨葡萄糖酸镁心肌保护作用的机理。方法 采用整体大鼠急性心肌缺血再灌注损伤模型 ,结扎冠脉左室前降支 4 0min后 ,再灌注 4 0min ,应用硝酸还原酶法测定血清中NO浓度 ,化学测定法测定血清中Mg2 + 含量 ,离子电极直接测定法测定组织内Ca2 + 浓度 ,采用硫代巴比妥钠 (TAB)比色法测定组织内MDA含量。结果 与假手术组相比 ,缺血再灌注损伤组血中NO浓度显著降低 ,组织内Ca2 + 浓度和MDA含量明显升高。与缺血损伤组相比 ,葡萄糖酸镁三个不同剂量保护组血中NO浓度明显升高 ,组织内Ca2 + 浓度和MDA含量明显降低 ,差异具有显著性 (P <0 0 5或P <0 0 1) ,此作用均可见明显剂量依赖性。结论 葡萄糖酸镁对心肌缺血再灌注损伤有保护作用 ,其保护作用机制与增加NO浓度、减轻钙超载和抗脂质过氧化有关。 Objective This paper was designed to observe the concentration change of NO and to investigate the cardioprotective effect of magnesium gluconate during myocardial ischemia reperfusion injury in anesthetized rats. Methods We adopted the model of myocardial ischemia reperfusion injury in anesthetized rats, assaied the concentration of NO and Mg^(2+) in blood serum, and we assaied the contents of Malondialdehyde (MDA) and Ca^(2+) in myocardium in the same time. Results Concentration of NO was decreased and MDA and Ca^(2+) contents were increased in the ischemia reperfusion group controed with sham, and concentration of NO was increased and MDA and Ca^(2+) contents were significantly decreased in the three different dosages group of magnesium gluconate controed with the ischemia reperfusion group. The dosage dependence was observed of the effect mentioned above. Conclusions Magnesium gluconate has protective effects on myocardial ischemia reperfusion injury .The protective effect may be related to increasing concentration of NO, relieving calcium overload and antilipid peroxidation.
出处 《锦州医学院学报》 2004年第5期15-18,共4页 Journal of Jinzhou Medical College
关键词 葡萄糖酸镁 心肌缺血再灌注损伤 NO MDA Magnesium gluconate myocardial ischemia reperfusion injury NO MDA
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参考文献3

  • 1Engelman DT.Constitutire nitric oxide release is impaired after ischemia and reperfusion. J Thorac Cardiovasc Surg[J].1995,110:1047-1053.
  • 2Woditsch I.Glyceryl triritrate but not sportaneows NO donors preserve myocardial function and cell mtegrity in ischemic rabbit hearts[J]. Agents Actions Supp,1995,45:189-194.
  • 3Feng QP, Hedner T. Endothelium-derived relaxing factor(EDRF) and nitric oxide(NO): physiology, pharmacology, and pathophysiology implications [J].Clin Physiol,1990,10:407-426.

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