摘要
肺内皮中一氧化氮(NO)通路的改变导致血管平滑肌张力增加和血管重塑,从而促进了肺动脉高压(PAH)的发展和进展。内皮NO合酶(eNOS)的表达减少和功能障碍以及阻止eNOS功能的因素的积累消除了肺NO信号传导。可以通过检测呼出气中的一氧化氮或测量血液或尿液中NO的降解产物(亚硝酸盐,硝酸盐,S-亚硝基硫醇)来评估肺血管系统的NO缺乏症。这些非侵入性生物标志物可能显示出与肺血流动力学变化相关并预测对治疗反应的潜力。当前的药物疗法旨在通过抑制NO的降解(磷酸二酯酶-5抑制剂)或增加内皮环鸟苷单磷酸的形成来刺激肺部NO信号传导,后者介导该途径的下游作用(可溶性鸟苷酸环化酶敏化剂)。最新数据支持亚硝酸盐化合物和富含硝酸盐的膳食补充剂可能会增加肺NO的利用率并降低血管阻力。这篇综述总结了关于NO途径参与PAH发病机制的当前知识,探索了肺NO的新颖且易于检测的生物标志物。
关键词: 肺动脉高压,一氧化氮,一氧化氮合酶,FENO,生物标志物,系统性硬化症。
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