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首页> 外文期刊>American Journal of Physiology >Increased inactivation of nitric oxide is involved in impaired coronary flow reserve in heart failure.
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Increased inactivation of nitric oxide is involved in impaired coronary flow reserve in heart failure.

机译：一氧化氮的失活增加与心力衰竭中冠状动脉血流储备受损有关。

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摘要

Recent evidence suggests that increased inactivation of endothelium-derived nitric oxide (NO) by oxygen free radical (OFR) formation is involved in the pathogenesis of endothelial dysfunction in heart failure (HF). However, it is unclear whether increased OFR limits coronary flow reserve in HF. To test this hypothesis, we examined the effects of antioxidant therapy on coronary flow reserve in a canine model of tachycardia-induced HF. The flow reserve (percent increase in coronary blood flow) to adenosine or to 20-s ischemia was less and OFR formation (electron-spin resonance spectroscopy) in myocardial tissues was greater in HF dogs than in controls. Immunohistochemical staining of 4-hydroxy-2-nonenal, an OFR-induced lipid peroxide, was detected in coronary microvessels of HF dogs. Intracoronary infusion of a cell-permeable OFR scavenger, tiron, suppressed OFR formation and improved the vasodilating capacity to adenosine or brief ischemia in HF dogs but not in controls. A NO synthesis inhibitor, N(G)-monomethyl-L-arginine (L-NMMA), diminished the beneficial effects of tiron in HF dogs. Vasodilation to sodium nitroprusside was similar between control and HF dogs, and no change in its response was noted with tiron or tiron + L-NMMA in either group. In summary, antioxidant treatment with tiron improved coronary flow reserve by increasing NO bioactivity in HF dogs. Thus increased OFR formation may impair coronary flow reserve in HF by reducing NO bioactivity.
机译：最近的证据表明，由氧自由基（OFR）形成的内皮源性一氧化氮（NO）失活增加与心力衰竭（HF）的内皮功能障碍的发病机理有关。但是，尚不清楚增加的OFR是否会限制HF中的冠状动脉血流储备。为了验证该假设，我们在心动过速诱发的心房颤动犬模型中研究了抗氧化剂治疗对冠状动脉血流储备的影响。与对照组相比，HF犬心肌组织中腺苷或20秒缺血的血流储备（冠状动脉血流增加百分比）更少，心肌组织中的OFR形成（电子自旋共振光谱法）更大。在HF狗的冠状微血管中检测到4-羟基-2-壬烯醛（一种由OFR诱导的脂质过氧化物）的免疫组织化学染色。冠状动脉内输注可透过细胞的OFR清道夫，铁剂，抑制了OFR的形成并改善了HF狗对腺苷或短暂缺血的血管舒张能力，但未在对照组中进行。 NO合成抑制剂N（G）-单甲基-L-精氨酸（L-NMMA）减少了铁剂对HF狗的有益作用。对照犬和HF犬之间，对硝普钠的血管舒张作用相似，并且在任何一组中，使用tiron或tiron + L-NMMA均未观察到其反应的变化。总之，用铁剂进行抗氧化剂治疗可通过增加HF狗的NO生物活性来改善冠状动脉血流储备。因此，增加的OFR形成可能会通过降低NO生物活性而损害HF中的冠状动脉血流储备。

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