Scherrer U, Vollenweider L, Delabays A, Savcic M, Eichenberger U, Kleger G R, Fikrle A, Ballmer P E, Nicod P, Bärtsch P
Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
N Engl J Med. 1996 Mar 7;334(10):624-9. doi: 10.1056/NEJM199603073341003.
Pulmonary hypertension is a hallmark of high-altitude pulmonary edema and may contribute to its pathogenesis. When administered by inhalation, nitric oxide, an endothelium-derived relaxing factor, attenuates the pulmonary vasoconstriction produced by short-term hypoxia.
We studied the effects of inhaled nitric oxide on pulmonary-artery pressure and arterial oxygenation in 18 mountaineers prone to high-altitude pulmonary edema and 18 mountaineers resistant to this condition in a high altitude laboratory (altitude, 4559 m). We also obtained lung-perfusion scans before and during nitric oxide inhalation to gain further insight into the mechanism of action of nitric oxide.
In the high-altitude laboratory, subjects prone to high-altitude pulmonary edema had more pronounced pulmonary hypertension and hypoxemia than subjects resistant to high-altitude pulmonary edema. Arterial oxygen saturation was inversely related to the severity of pulmonary hypertension (r=-0.50, P=0.002). In subjects prone to high-altitude pulmonary edema, the inhalation of nitric oxide (40 ppm for 15 minutes) produced a decrease in mean (+/-SD) systolic pulmonary-artery pressure that was three times larger than the decrease in subjects resistant to such edema (25.9+/-8.9 vs. 8.7+/-4.8 mm Hg, P<0.001). Inhaled nitric oxide improved arterial oxygenation in the 10 subjects who had radiographic evidence of pulmonary edema (arterial oxygen saturation increased from 67+/-10 to 73+/-12 percent, P=0.047), whereas it worsened oxygenation in subjects resistant to high-altitude pulmonary edema. The nitric oxide-induced improvement in arterial oxygenation in subjects with high-altitude pulmonary edema was accompanied by a shift in blood flow in the lung away from edematous segments and toward nonedematous segments.
The inhalation of nitric oxide improves arterial oxygenation in high-altitude pulmonary edema, and this beneficial effect may be related to its favorable action on the distribution of blood flow in the lungs. A defect in nitric nitric oxide synthesis may contribute to high-altitude pulmonary edema.
肺动脉高压是高原肺水肿的一个标志，可能参与其发病机制。一氧化氮作为一种内皮源性舒张因子，经吸入给药时，可减轻短期缺氧所致的肺血管收缩。
在一个高海拔实验室（海拔4559米）中，我们研究了吸入一氧化氮对18名易患高原肺水肿的登山者和18名对该病有抵抗力的登山者的肺动脉压和动脉氧合的影响。我们还在吸入一氧化氮之前和期间进行了肺灌注扫描，以进一步了解一氧化氮的作用机制。
在高海拔实验室中，易患高原肺水肿的受试者比有高原肺水肿抵抗力的受试者有更明显的肺动脉高压和低氧血症。动脉血氧饱和度与肺动脉高压的严重程度呈负相关（r = -0.50，P = 0.002）。在易患高原肺水肿的受试者中，吸入一氧化氮（40 ppm，持续15分钟）使平均（±标准差）收缩期肺动脉压的降低幅度比有抵抗力的受试者大三倍（25.9±8.9 vs. 8.7±4.8 mmHg，P<0.001）。吸入一氧化氮改善了10名有肺水肿影像学证据的受试者的动脉氧合（动脉血氧饱和度从67±10%增加到73±12%，P = 0.047），而在有高原肺水肿抵抗力的受试者中，它使氧合恶化。一氧化氮诱导的有高原肺水肿受试者的动脉氧合改善伴随着肺内血流从水肿段向非水肿段的转移。
吸入一氧化氮可改善高原肺水肿患者的动脉氧合，这种有益作用可能与其对肺内血流分布的有利作用有关。一氧化氮合成缺陷可能导致高原肺水肿。
