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Departments of Medicine and Radiology, University of Bern, Inselspital, CH-3010 Bern; Department of Medicine, Kantonsspital, CH-7000 Chur, Switzerland; Departments of Sports Medicine and Hematology, University of Heidelberg, D-69115 Heidelberg, Germany; and Departments of Pharmacology and Medicine, Vanderbilt University, Nashville, Tennessee 37232-6602
Received 10 November 1995; accepted in final form 25 June 1996.
Kleger, Gian-Reto, Peter Bärtsch, Peter Vock, Bernhard
Heilig, L. Jackson Roberts II, and Peter E. Ballmer. Evidence against an increase in capillary permeability in subjects exposed to
high altitude. J. Appl. Physiol.
81(5): 1917-1923, 1996.
A potential pathogenetic cofactor for the
development of acute mountain sickness and high-altitude pulmonary
edema is an increase in capillary permeability, which could occur as a
result of an inflammatory reaction and/or free radical-mediated
injury to the lung. We measured the systemic albumin escape by
intravenously injecting 5 µCi of 125I-labeled albumin and the
plasma concentrations of cytokines, F2-isoprostanes (products of lipid
peroxidation), and acute-phase proteins in 24 subjects exposed to 4,559 m. Ten subjects developed acute mountain sickness, and four subjects
developed high-altitude pulmonary edema. The transcapillary escape
rate of albumin was 6.9 ± 2.0%/h (SD) at low (550 m) and 6.3 ± 1.9%/h at high (4,559 m) altitude (P = 0.23; n = 24). The subjects with
high-altitude pulmonary edema had a modest but insignificant increase
in the transcapillary escape rate of albumin (4.6 ± 1.9%/h at low
vs. 5.7 ± 1.9%/h at high altitude;
P = 0.42;
n = 4). Plasma concentrations of
fibrinogen, 
1-acid
glycoprotein, C-reactive protein, and interleukin-6 were unchanged in
the early phases and significantly increased by the end of the
observation period in the subjects with high-altitude pulmonary edema,
whereas tumor necrosis factor- and
F2-isoprostanes did not change at
all. This suggests that the inflammatory reaction was rather a
consequence than a causative factor of high-altitude pulmonary edema.
In summary, these data argue against a dominant role for increased
systemic capillary permeability in the development of acute mountain
sickness and high-altitude pulmonary edema.
vascular permeability; high-altitude pulmonary edema; acute mountain sickness; free radicals; F2-isoprostanes
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