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Inhaled nitric oxide for high-altitude pulmonary edema
U Scherrer1, L Vollenweider, A Delabays
1Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
The New England Journal of Medicine
|March 7, 1996
Summary
Inhaled nitric oxide (NO) improves oxygen levels in individuals with high-altitude pulmonary edema by redirecting blood flow. A deficiency in NO synthesis may play a role in developing this condition.
Area of Science:
- Cardiovascular Physiology
- Altitude Medicine
- Respiratory Physiology
Background:
- Pulmonary hypertension is a key feature of high-altitude pulmonary edema (HAPE).
- Inhaled nitric oxide (NO), a vasodilator, can counteract hypoxic pulmonary vasoconstriction.
- Understanding NO's role in HAPE is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the effects of inhaled nitric oxide on pulmonary artery pressure and arterial oxygenation in individuals with and without HAPE.
- To explore the mechanism of NO's action using lung-perfusion scans.
Main Methods:
- Studied 36 mountaineers (18 prone to HAPE, 18 resistant) at 4559m altitude.
- Administered inhaled nitric oxide (40 ppm for 15 minutes).
- Monitored pulmonary artery pressure, arterial oxygenation, and performed lung-perfusion scans.
Main Results:
- Individuals prone to HAPE exhibited greater pulmonary hypertension and hypoxemia.
- Inhaled NO significantly reduced pulmonary artery pressure in HAPE-prone individuals compared to resistant individuals.
- NO improved arterial oxygenation in HAPE subjects by redistributing lung blood flow away from edematous areas.
Conclusions:
- Inhaled nitric oxide benefits arterial oxygenation in HAPE, likely via improved pulmonary blood flow distribution.
- Potential defects in nitric oxide synthesis may contribute to the pathogenesis of HAPE.