NO在外源性高浓度Ca2+损伤心肌线粒体中的作用

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20 μmol/L EDTA、100 μmol/L CaCl₂以及1 μmol/L L-NAME+100 μmol/L CaCl₂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NO₂^-/NO₃^-含量呈显著负相关（r=-0.5297，P<0.01；r=-0.6041，P<0.01）；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NO₂^-/NO₃^-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。

Effects of nitric oxide on mitochondrial damage caused by exogenous calcium

AIM: To study the effects of nitric oxide (NO) on mitochondrial damage caused by exogenous calcium. METHODS: Normal myocardial mitochondria were divided into three groups; L- arginine control group (CG), Ca2 + - damaged group (DG) and L - NAME - preserved group (PG). Mitochondria of all groups were incubated at 30℃ with reaction medium containing 20μmol/L EDTA, 100μmol/L CaC12 and 1 μmol/L L- NAME with 100μmol/L CaCl2 respectively. Then the NO2-/NO3- contents, mitochondrial viability and membrane potential were investigated. RESULTS: The NO2-/NO3 contents of DG was obviously higher than that of CG and PG, meanwhile, there was no obvious difference between CG and PG. Mitochondrial viability and membrane potential of DG were significantly lower than that of CG and PG, and negatively related to NO2-/NO3- contents ( r = - 0.5297, P < 0.01; r = -0.6041, P < 0.01 ). But, the mitochondrial viability and membrane potential of PG were still lower than that of CG. CONCLUSION: Exogenous calcium could activate mitochondrial nitric oxide synthase resulting in NO production and the latter play an important role in decreasing mitochondrial viability and membrane potential.