ISSN:
1439-6327
Keywords:
Key words Lung vascular permeability
;
Inflammation
;
Cytokines
;
Altitude
;
Vascular endothelial growth factor
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract In order to investigate whether vascular endothelial growth factor (VEGF) and inflammatory pathways are activated during acute hypobaric hypoxia in subjects who are susceptible to high-altitude pulmonary oedema (HAPE-S), seven HAPE-S and five control subjects were exposed to simulated altitude corresponding to 4000 m in a hypobaric chamber for 1 day. Peripheral venous blood was taken at 450 m (Zürich level) and at 4000 m, and levels of erythropoietin (EPO), VEGF, interleukin-6 (IL-6) and the acute-phase proteins complement C3 (C3), α1-antitrypsin (α1AT), transferrin (Tf ) and C-reactive protein (CRP) were measured. Peripheral arterial oxygen saturation (S aO2) was recorded. Chest radiography was performed before and immediately after the experiment. EPO increased during altitude exposure, correlating with S aO2, in both groups (r = −0.86, P 〈 0.001). Venous serum VEGF did not show any elevation despite a marked decrease in S aO2 in the HAPE-S subjects [mean (SD) HAPE-S: 69.6 (9.1)%; controls: 78.7 (5.2)%]. C3 and α1AT levels increased in HAPE-S during hypobaric hypoxia [from 0.94 (0.11) g/l to 1.07 (0.13) g/l, and from 1.16 (0.08) g/l to 1.49 (0.27) g/l, respectively; P 〈 0.05], but remained within the clinical reference ranges. No significant elevations of IL-6, Tf or CRP were observed in either group. The post-exposure chest radiography revealed no signs of oedema. We conclude that VEGF is not up-regulated in HAPE-S and thus does not seem to increase critically pulmonary vascular permeability during the 1st day at high altitude. Furthermore, our data provide evidence against a clinically relevant inflammation in the initial phase of exposure to hypoxia in HAPE-S, although C3 and α1AT are mildly induced.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/s004210050074
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