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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Reduction of nitrite to nitric oxide during ischemia protects against myocardial ischemia-reperfusion damage
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Reduction of nitrite to nitric oxide during ischemia protects against myocardial ischemia-reperfusion damage

机译：在缺血期间将亚硝酸盐还原为一氧化氮可防止心肌缺血-再灌注损伤

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摘要

Nitric oxide (NO.) is thought to protect against the damaging effects of myocardial ischemia-reperfusion injury, whereas xanthine oxidoreductase (XOR) normally causes damage through the generation of reactive oxygen species. In the heart, inorganic nitrite (NO2-) has the potential to act as an endogenous store of NO. liberated specifically during ischemia. Using a detection method that we developed, we report that under ischemic conditions both rat and human homogenized myocardium and the isolated perfused rat heart (Langendorff preparation) generate NO. from NO2- in a reaction that depends on XOR activity. Functional studies of rat hearts in the Langendorff apparatus showed that nitrite (10 and 100 muM) reduced infarct size from 47.3 +/- 2.8% (mean percent of control +/- SEM) to 17.9 +/- 4.2% and 17.4 +/- 1.0%, respectively (P < 0.001), and was associated with comparable improvements in recovery of left ventricular function. This protective effect was completely blocked by the NO. scavenger 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazole-1-oxyl 3-oxide (carboxy-PTIO). In summary, the generation of NO. from NO2-, by XOR, protects the myocardium from ischemia-reperfusion injury. Hence, if XOR is presented with NO2- as an alternative substrate, the resultant effects of its activity may be protective, by means of its production of NO., rather than damaging.
机译：一氧化氮（NO。）被认为可以防止心肌缺血-再灌注损伤的破坏作用，而黄嘌呤氧化还原酶（XOR）通常通过产生活性氧而引起损害。在心脏中，无机亚硝酸盐（NO2-）可能充当NO的内源性存储。在缺血过程中特别释放。使用我们开发的检测方法，我们报告说，在缺血条件下，大鼠和人的均质心肌以及分离的灌注大鼠心脏（Langendorff制剂）均会产生NO。在取决于XOR活性的反应中由NO2-生成。在Langendorff装置中对大鼠心脏进行的功能研究表明，亚硝酸盐（10和100μM）将梗塞面积从47.3 +/- 2.8％（相对于对照组+/- SEM的平均百分比）降低到17.9 +/- 4.2％和17.4 +/-分别为1.0％（P <0.001），并且与左心室功能恢复的可比改善有关。 NO完全阻止了这种保护作用。清除剂2-（4-羧基苯基）-4,4,5,5-四甲基咪唑-1-氧基3-氧化物（羧基-PTIO）。综上所述，NO的产生。 XOR的NO2-可以保护心肌免受缺血再灌注损伤。因此，如果将XOR与NO2-作为替代底物一起使用，则其活性所产生的最终效果可能会通过生成NO。而起到保护作用，而不是造成损害。

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