Hypoxia decreases exhaled nitric oxide in mountaineers susceptible to high-altitude pulmonary edema
Hypoxia decreases exhaled nitric oxide in mountaineers susceptible to high-altitude pulmonary edema
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DOI：
10.1164/ajrccm.163.2.2001134
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发表时间：
2001-02-01
影响因子：
24.7
通讯作者：
Swenson, ER
中科院分区：
文献类型：
--
作者：
Busch, T;Bärtsch, P;Swenson, ER
过度的缺氧性肺血管收缩对于高原肺水肿（HAPE）的发生至关重要。我们假设，敏感性ttl HAPE可能与减少一氧化氮（NO），肺血管阻力的内源性调节剂的生产，并在呼出的NO减少，可以检测到在缺氧暴露。因此，我们研究了呼吸道NO分泌的化学发光和肺动脉收缩压（Ppa，s）的超声心动图在9个HAPE敏感的登山者和9个HAPE抵抗的对照组在常氧和急性缺氧（分数吸入氧[Fi（O2）] = 0.12）。受试者进行经口呼吸。通过鼻罩抽吸将鼻排出的NO与呼吸气体分离。在HAPE易感受试者中，与常氧相比，在缺氧2 h期间呼出气体中的NO排出显著降低（p < 0.05）（28 +/- 4 vs 21 +/-2nl/min，平均值+/- SEM）。相反，对照组受试者的NO排泄率保持不变（31 +/- 6 vs 33 +/- 6 nl/ min，NS）。在常氧条件下，两组之间的鼻NO排泄量无显著差异（HAPE敏感组，183 +/- 16 nl/ min;对照组，297 +/- 55 nl/min，NS），且不受缺氧影响。缺氧时Ppa，s的变化与Tower呼吸道NO排泄的百分比变化相关（R =-0.49，p = 0.04）。我们的数据提供了第一个证据表明，在急性缺氧期间，HAPE易感受试者的肺NO产生减少，这可能是导致其缺氧肺血管反应增强的因素之一。
An exaggerated hypoxic pulmonary vasoconstriction is essential for development of high-altitude pulmonary edema (HAPE). We hypothesized that susceptibility ttl HAPE may be related to decreased production of nitric oxide (NO), an endogenous modulator of pulmonary vascular resistance, and that a decrease in exhaled NO could be detected during hypoxic exposure. Therefore, we investigated respiratory tract NO excretion by chemiluminescence and pulmonary artery systolic pressure (Ppa,s) by echocardiography in nine HAPE-susceptible mountaineers and nine HAPE-resistant control subjects during normoxia and acute hypoxia (fraction of inspired oxygen [Fi(O2)] = 0.12). The subjects performed oral breathing. Nasally excreted NO was separated from respiratory gas by suction via a nasal mask, in HAPE-susceptible subjects, NO excretion in expired gas significantly decreased (p < 0.05) during hypoxia of 2 h in comparison with normoxia (28 +/- 4 versus 21 +/- 2 nl/min, mean +/- SEM). In contrast, the NO excretion rate of control subjects remained unchanged (31 +/- 6 versus 33 +/- 6 nl/ min, NS). Nasal NO excretion did not differ significantly between groups during normoxia (HAPE-susceptible group, 183 +/- 16 nl/ min; control subjects, 297 +/- 55 nl/min, NS) and was not influenced by hypoxia. The changes in Ppa,s with hypoxia correlated with the percent changes in Tower respiratory tract NO excretion (R = -0.49, p = 0.04). Our data provide the first evidence of decreased pulmonary NO production in HAPE-susceptible subjects during acute hypoxia that may contribute among other factors to their enhanced hypoxic pulmonary vascular response.