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Background: Exposure to hypobaric hypoxemia causes acute mountain sickness (AMS) in 40% of subjects acutely exposed to an altitude of 4,000 m. Vascular endothelial growth factor (VEGF) and cytokines appear to play a role in AMS in model systems. The objective of this pilot study was to explore the change in VEGF, the vasodilatory prostacyclin PGI-2, interleukin-6 and thiobarbituric acid reactive substances (TBARS) levels following prolonged exposure to hypobaric hypoxemia on Bolivian Altiplano. The secondary objective was to investigate the relationship between these markers with good versus poor adaptation to high altitude.  Methods: The study population consisted of 7 climbers aged 24-64 yr. One cardiac transplant and one kidney transplant recipients participated in this study. Aerobic capacity was assessed on a treadmill using a RAMP protocol with gas exchange analyses. Blood samples were harvested within 48 hr of departure and within 24 hr returning to sea level.  Results: Selected biochemisty parameters are presented in the table:   *** Table in Full Text PDF. ***  Data are mean ±SD. CP= cardiopulmonary. Both cardiac and Tx recipients did not experience AMS. Maximum altitude achieved: ∗6120-6522; †5680; ‡5300 meters.  Conclusions: Pulmonary maladaptation to high altitude results in a 2-fold elevated VEGF and PGI-2 without concomitant increase of markers of inflammation or oxidative stress. VEGF does not appear to increase in cerebral maladaptation to high altitude. Further investigations are needed to better understand the role of VEGF and other biomarkers during the process of adaptation or maladaptation to high altitude.

Persistent Elevation of Vascular Endothelial Growth Factor and Prostacyclin Following Cardiopulmonary Maladaptation to High Altitude: A Pilot study