Exhaled nitric oxide in high-altitude pulmonary edema - Role in the regulation of pulmonary vascular tone and evidence for a role against inflammation
Exhaled nitric oxide in high-altitude pulmonary edema - Role in the regulation of pulmonary vascular tone and evidence for a role against inflammation
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DOI：
10.1164/ajrccm.162.1.9908039
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发表时间：
2000-07-01
影响因子：
24.7
通讯作者：
Scherrer, U
中科院分区：
文献类型：
--
作者：
Duplain, H;Sartori, C;Scherrer, U
高原肺水肿 (HAPE) 是一种危及生命的疾病，发生在海拔 2,500 m 以上的易感人群中。目前尚不清楚，除了血流动力学因素和肺泡液清除缺陷之外，炎症是否在 HARE 中起着致病作用。因此，我们对 28 名 HAPE 易发者和 24 名对照受试者在高海拔暴露 (4,559 m) 期间进行了呼出的肺一氧化氮 (NO)（气道炎症标志物）的连续测量。为了检查肺一氧化氮合成和肺血管张力之间的关系，我们还测量了肺动脉收缩压（Ppa）。在 13 名发生 HAPE 的受试者中，呼出的 NO 在肺水肿发生过程中没有表现出任何增加的趋势。在整个高海拔逗留期间，易患野兔的肺部呼出一氧化氮比对照组低约 30%，并且 Ppa 和呼出一氧化氮之间存在负相关关系（r = -0.51，p < 0.001）。这些发现表明，HARE 之前并不存在气道炎症。呼出一氧化氮减少可能与肺一氧化氮合成和/或运输和清除的改变有关，我们研究中的数据可能与新概念一致，即在易患HAPE的受试者中，肺上皮一氧化氮合成缺陷可能导致过度缺氧性肺血管收缩，进而导致肺水肿。
High-altitude pulmonary edema (HAPE) is a life-threatening condition occurring in predisposed subjects at altitudes above 2,500 m. It is not clear whether, in addition to hemodynamic factors and defective alveolar fluid clearance, inflammation plays a pathogenic role in HARE. We therefore made serial measurements of exhaled pulmonary nitric oxide (NO), a marker of airway inflammation, in 28 HAPE-prone and 24 control subjects during high-altitude exposure (4,559 m). To examine the relationship between pulmonary NO synthesis and pulmonary vascular tone, we also measured systolic pulmonary artery pressure (Ppa). In the 13 subjects who developed HAPE, exhaled NO did not show any tendency to increase during the development of lung edema. Throughout the entire sojourn at high altitude, pulmonary exhaled NO was roughly 30% lower in HARE-prone than in control subjects, and there existed an inverse relationship between Ppa and exhaled NO (r = -0.51, p < 0.001). These findings suggest that HARE is not preceded by airway inflammation. Reduced exhaled NO may be related to altered pulmonary NO synthesis and/or transport and clearance, and the data in our study could be consistent with the novel concept that in HAPE-prone subjects, a defect in pulmonary epithelial NO synthesis may contribute to exaggerated hypoxic pulmonary vasoconstriction and in turn to pulmonary edema.