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Original Article
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Volume 334:624-630 March 7, 1996 Number 10
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Inhaled Nitric Oxide for High-Altitude Pulmonary Edema
Urs Scherrer, M.D., Laurent Vollenweider, M.D., Alain Delabays, M.D., Milos Savcic, M.D., Urs Eichenberger, M.D., Gian-Reto Kleger, M.D., Antonin Fikrle, M.D., Peter E. Ballmer, M.D., Pascal Nicod, M.D., and Peter Bärtsch, M.D.

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ABSTRACT

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 oxide synthesis may contribute to high-altitude pulmonary edema.


Source Information

From the Department of Internal Medicine (U.S., P.N.) and the Division of Cardiology (A.D., M.S.), Centre Hospitalier Universitaire Vaudois, Lausanne; the Institute of Physiology, Lausanne (L.V.); and the Departments of Medicine (G.-R.K., P.E.B.), Radiology (U.E.), and Nuclear Medicine (A.F.), University Hospital, Berne — all in Switzerland; and the Department of Sports Medicine, University of Heidelberg, Heidelberg, Germany (P.B.). Presented in part at the 67th Scientific Sessions of the American Heart Association, Dallas, November 14–17, 1994, and at the 9th International Hypoxia Symposium at Lake Louise, Alta., Canada, February 14–18, 1995.

Address reprint requests to Dr. Scherrer at the Department of Internal Medicine, BH 10.642, CHUV, 1011 Lausanne, Switzerland.

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