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1 Department of Physiology, Free University of Brussels, B1070 Brussels, Belgium; 2 Faculty of Health Sciences, University of Copenhagen, DK-2000 Copenhagen N, Denmark; 3 Department of Intensive Care Medicine, Erasme Hôspital, B1070 Brussels, Belgium; 4 National Center for Cardiology and Internal Medicine, Bishkek, Kyrgyzstan; 5 Department of Medical Physics, Royal Hallamshire Hospital, Sheffield S10 2JF, United Kingdom
Recent work suggests that
treatment with inhaled
2-agonists reduces the incidence
of high-altitude pulmonary edema in susceptible subjects by increasing
respiratory epithelial sodium transport. We estimated respiratory
epithelial ion transport by transepithelial nasal potential difference
(NPD) measurements in 20 normal male subjects before, during, and after
a stay at 3,800 m. NPD hyperpolarized on ascent to 3,800 m
(P < 0.05), but the change in potential difference with superperfusion of amiloride or isoprenaline was unaffected. Vital
capacity (VC) fell on ascent to 3,800 m (P < 0.05), as
did the normalized change in electrical impedance (NCI) measured over the right lung parenchyma (P < 0.05) suggestive of an
increase in extravascular lung water. Echo-Doppler-estimated pulmonary artery pressure increases were insufficient to cause clinical pulmonary
edema. There was a positive correlation between VC and NCI
(R2 = 0.633) and between NPD and both VC
and NCI (R2 = 0.267 and 0.418). These
changes suggest that altered respiratory epithelial ion transport might
play a role in the development of subclinical pulmonary edema at high
altitude in normal subjects.
pulmonary edema; hypobaric hypoxia
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