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首页> 外文期刊>Circulation: An Official Journal of the American Heart Association >Folic acid prevents nitroglycerin-induced nitric oxide synthase dysfunction and nitrate tolerance: a human in vivo study.
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Folic acid prevents nitroglycerin-induced nitric oxide synthase dysfunction and nitrate tolerance: a human in vivo study.

机译：叶酸可防止硝酸甘油诱导的一氧化氮合酶功能障碍和硝酸盐耐受性：一项人体体内研究。

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BACKGROUND: In healthy humans, continuous treatment with nitroglycerin (GTN) causes nitric oxide synthase dysfunction, probably through the reduced bioavailability of tetrahydrobiopterin. Recent studies proposed that folic acid is involved in the regeneration of tetrahydrobiopterin in different disease states. Therefore, we investigated whether folic acid administration would prevent this phenomenon. We also sought to determine if folic acid supplementation could prevent the development of tolerance to GTN. METHODS AND RESULTS: On the first visit, 18 healthy male volunteers (aged 19 to 32 years) were randomized to receive either oral folic acid (10 mg once a day) or placebo for 1 week in a double-blind designed study. All subjects also received continuous transdermal GTN (0.6 mg/h). On the second visit, forearm blood flow was measured with venous occlusion strain gauge plethysmography in response to incremental infusions of acetylcholine (7.5, 15, and 30 microgram/min), N-monomethyl-L-arginine (1, 2, and 4 micromol/min), and GTN (11 and 22 nmol/min). Folic acid prevented GTN-induced endothelial dysfunction, as assessed by responses to intraarterial acetylcholine and N-monomethyl-L-arginine (P<0.01). Moreover, in the subjects treated with folic acid plus transdermal GTN, responses to intraarterial GTN were significantly greater than those observed after transdermal GTN plus placebo (P<0.05). CONCLUSION: Our data demonstrate that supplemental folic acid prevents both nitric oxide synthase dysfunction induced by continuous GTN and nitrate tolerance in the arterial circulation of healthy volunteers. We hypothesize that the reduced bioavailability of tetrahydrobiopterin is involved in the pathogenesis of both phenomena. Our results confirm the view that oxidative stress contributes to nitrate tolerance.
机译：背景：在健康的人类中，连续使用硝酸甘油（GTN）治疗可能导致一氧化氮合酶功能异常，这可能是由于四氢生物蝶呤的生物利用度降低所致。最近的研究提出叶酸在不同疾病状态下参与四氢生物蝶呤的再生。因此，我们调查了叶酸给药是否可以预防这种现象。我们还试图确定补充叶酸是否可以阻止对GTN的耐受性的发展。方法和结果：首次访问时，在双盲设计研究中，随机将18名健康的男性志愿者（年龄在19至32岁之间）随机接受口服叶酸（每天一次10 mg）或安慰剂1周。所有受试者还接受了连续的透皮GTN（0.6 mg / h）。在第二次就诊时，对乙酰胆碱（7.5、15和30微克/分钟），N-单甲基-L-精氨酸（1、2和4微摩尔）的增量输注，采用静脉阻塞应变仪体积描记法测量前臂血流量/ min）和GTN（11和22 nmol / min）。通过对动脉内乙酰胆碱和N-单甲基-L-精氨酸的反应评估，叶酸可预防GTN诱导的内皮功能障碍（P <0.01）。此外，在接受叶酸加经皮GTN治疗的受试者中，对动脉内GTN的反应明显高于经皮GTN加安慰剂后所观察到的反应（P <0.05）。结论：我们的数据表明，补充叶酸既可以防止连续GTN引起的一氧化氮合酶功能障碍，又可以防止健康志愿者的动脉循环中的硝酸盐耐受性。我们假设四氢生物蝶呤的生物利用度降低与这两种现象的发病机理有关。我们的结果证实了氧化应激有助于硝酸盐耐受性的观点。

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