Inhaled Nitric Oxide for High-altitude Pulmonary Edema
Overview
Authors
Affiliations
Background: 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.
Methods: 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.
Results: 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.
Conclusions: 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.
Wang C, Mao Z, Gomchok D, Li X, Liu H, Shao J Heliyon. 2025; 11(2):e41960.
PMID: 39906863 PMC: 11791212. DOI: 10.1016/j.heliyon.2025.e41960.
High altitude pulmonary oedema: Mimicker of acute coronary syndrome.
Jain R, Sengupta S, Sharma A, Mishra Y Med J Armed Forces India. 2024; 80(Suppl 1):S312-S319.
PMID: 39734830 PMC: 11670623. DOI: 10.1016/j.mjafi.2023.07.014.
Feasibility of Delivering 5-Day Normobaric Hypoxia Breathing in a Hospital Setting.
Berra L, Medeiros K, Marrazzo F, Patel S, Imber D, Rezoagli E Respir Care. 2024; 69(11):1400-1408.
PMID: 39079724 PMC: 11549621. DOI: 10.4187/respcare.11928.
Hanaoka M, Kobayashi T, Droma Y, Ota M, Kobayashi N, Wada Y Intern Med. 2024; 63(17):2355-2366.
PMID: 38171855 PMC: 11442931. DOI: 10.2169/internalmedicine.2533-23.
Hannemann J, Freytag J, Schiefer L, Macholz F, Sareban M, Schmidt-Hutten L Front Physiol. 2023; 14:1297636.
PMID: 38093907 PMC: 10716225. DOI: 10.3389/fphys.2023.1297636.