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Published on: May 11, 2015
Exaggerated endothelin release in high-altitude pulmonary edema
C Sartori1, L Vollenweider, B M Löffler
1Department of Internal Medicine, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
Circulation
|May 25, 1999
Summary
Mountaineers susceptible to high-altitude pulmonary edema (HAPE) show higher endothelin-1 levels, a peptide causing pulmonary vasoconstriction. This suggests endothelin-1 contributes to HAPE by increasing pulmonary hypertension at high altitudes.
Area of Science:
- Altitude Medicine
- Cardiovascular Physiology
- Pulmonary Hypertension Research
Background:
- Pulmonary hypertension is implicated in high-altitude pulmonary edema (HAPE) pathogenesis.
- Endothelin-1, a potent vasoconstrictor, increases microvascular permeability.
Purpose of the Study:
- To investigate the role of endothelin-1 in HAPE susceptibility.
- To compare endothelin-1 plasma levels and pulmonary artery pressure in HAPE-prone versus HAPE-resistant mountaineers at varying altitudes.
Main Methods:
- Measurement of endothelin-1 plasma levels and pulmonary artery pressure.
- Comparison between 16 HAPE-prone and 16 HAPE-resistant mountaineers.
- Data collection at low (580 m) and high (4559 m) altitudes.
Main Results:
- At high altitude, HAPE-prone mountaineers had ~33% higher endothelin-1 levels than HAPE-resistant individuals (22.2 vs. 16.8 pg/mL, P<0.01).
- A direct correlation was observed between changes in endothelin-1 levels and systolic pulmonary artery pressure (r=0.82, P<0.01).
- Endothelin-1 levels correlated with pulmonary artery pressure at high altitude (r=0.35, P=0.05).
Conclusions:
- Elevated endothelin-1 release or reduced clearance may contribute to exaggerated pulmonary hypertension in HAPE-susceptible individuals.
- Endothelin-1 is a potential mechanism underlying HAPE pathogenesis at high altitudes.
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