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目的 :探讨一氧化氮在外源性高浓度Ca2 + 损伤心肌线粒体中的作用。方法 :正常心肌线粒体分为单纯L -精氨酸 (L -Arg)组、Ca2 + 损伤组和左旋硝基精氨酸甲酯 (L -NAME)保护组 ,分别于含有 2 0 μmol/LEDTA、10 0 μmol/LCaCl2 以及 1μmol/LL -NAME +10 0 μmol/LCaCl2 的反应介质中孵育 ,然后测定线粒体活力、膜电位以及NO含量。结果 :Ca2 + 损伤组线粒体活力、膜电位明显下降 ,而NO-2 /NO-3 含量升高 ,且线粒体活力、膜电位与NO-2 /NO-3 含量呈显著负相关 (r=- 0 .5 2 97,P <0 0 1;r=- 0 6 0 41,P <0 0 1) ;L -NAME保护组线粒体活力与膜电位均明显高于Ca2 + 损伤组 ,但仍低于L -Arg组 ,而NO-2 /NO-3 含量低于Ca2 + 损伤组 ,且与L -Arg组无明显差异。结论 :外源性Ca2 + 可激活线粒体一氧化氮合酶 ,使NO生成增多 ,后者在线粒体活力与膜电位降低中起重要作用。
Objective: To investigate the role of nitric oxide in myocardial mitochondria induced by exogenous high concentration Ca2 +. Methods: The mitochondria of normal myocardium were divided into two groups: L - Arg group, Ca2 + group and L - NAME group, 10 0 μmol / L CaCl2 and 1 μmol / LL-NAME +10 0 μmol / L CaCl2. Then the mitochondrial activity, membrane potential and NO content were measured. Results: The mitochondrial viability and membrane potential were significantly decreased in Ca2 + injury group, while the content of NO-2 / NO-3 was increased. The mitochondrial activity and membrane potential were negatively correlated with NO-2 / NO- .5 2 97, P <0.01; r = - 0 6041, P <0.01). The mitochondrial vitality and membrane potential of L-NAME group were significantly higher than that of Ca2 + group but still lower than L -Arg group, while NO-2 / NO-3 content was lower than that of Ca2 + -induced group, and no significant difference with L-Arg group. CONCLUSION: Exogenous Ca2 + activates mitochondrial nitric oxide synthase and increases NO production, which plays an important role in mitochondrial activity and membrane potential reduction.