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Articles in PresS, published online ahead of print December 6, 2002
J Appl Physiol, 10.1152/jap.00777.2002
Submitted on August 26, 2002
Accepted on November 20, 2002
1 Department of Physiology, Free University of Brussels, Brussels, Belgium
2 Faculty of Health Sciences, University of Copenhagen, Copenhagen, Denmark
3 Department of Intensive Care Medicine, Erasme Hospital, Brussels, Belgium
4 National Centre for Cardiology and Internal Medicine, Bishkek, Kyrgyzstan
5 Department of Medical Physics, Royal Hallamshire Hospital, Sheffield, United Kingdom
* To whom correspondence should be addressed. E-mail: nmason{at}ulb.ac.be.
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 3800m. NPD hyperpolarized on ascent to 3800m (p<0.05) but the change in potential difference with superperfusion of amiloride or isoprenaline was unaffected. Vital capacity (VC) fell on ascent to 3800m (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.
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