(Circulation. 1999;99:2665-2668.)
© 1999 American Heart Association, Inc.
Clinical Investigation and Reports |
From the Department of Internal Medicine (C.S., P.N., U.S.) and Division of Cardiology (A.D.), Centre Hospitalier Universitaire Vaudois, Lausanne; Institute of Physiology (L.V.), University of Lausanne, Lausanne; Pharma Division Preclinical Research, F. Hoffmann-La Roche Ltd (B.-M.L.), Basel, Switzerland; and Department of Sports Medicine, University of Heidelberg, Heidelberg, Germany (P.B.).
Correspondence to Dr Urs Scherrer, Department of Internal Medicine, BH 10.642, Centre Hospitalier Universitaire Vaudois, CH-1011 Lausanne, Switzerland. E-mail Urs.Scherrer{at}chuv.hospvd.ch
BackgroundExaggerated pulmonary hypertension is thought to play an important part in the pathogenesis of high-altitude pulmonary edema (HAPE). Endothelin-1 is a potent pulmonary vasoconstrictor peptide that also augments microvascular permeability.
Methods and ResultsWe measured endothelin-1 plasma levels and
pulmonary artery pressure in 16 mountaineers prone to HAPE and
in 16 mountaineers resistant to this condition at low (580 m)
and high (4559 m) altitudes. At high altitude, in mountaineers prone to
HAPE, mean (±SE) endothelin-1 plasma levels were
33% higher than
in HAPE-resistant mountaineers (22.2±1.1 versus 16.8±1.1
pg/mL, P<0.01). There was a direct relationship between
the changes from low to high altitude in endothelin-1 plasma levels and
systolic pulmonary artery pressure
(r=0.82, P<0.01) and between
endothelin-1 plasma levels and pulmonary artery pressure
measured at high altitude (r=0.35,
P=0.05).
ConclusionsThese findings suggest that in HAPE-susceptible mountaineers, an augmented release of the potent pulmonary vasoconstrictor peptide endothelin-1 and/or its reduced pulmonary clearance could represent one of the mechanisms contributing to exaggerated pulmonary hypertension at high altitude.
Key Words: endothelin hypertension, pulmonary altitude edema hypoxia
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