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1 Separtment of Anesthesiology, University of Colorado Health Sciences Center, Denver, CO, USA; Colorado Center for Altitude Medicine and Physiology, University of Colorado Health Sciences Center, Denver, CO, USA
2 Exercise Physiology, Mesa State College, Grand Junction, CO, USA; Colorado Center for Altitude Medicine and Physiology, University of Colorado Health Sciences Center, Denver, CO, USA
3 Colorado Center for Altitude Medicine and Physiology, University of Colorado Health Sciences Center, Denver, CO, USA
4 Separtment of Anesthesiology, University of Colorado Health Sciences Center, Denver, CO, USA
* To whom correspondence should be addressed. E-mail: martha.tissotvanpatot{at}uchsc.edu.
Vascular endothelial growth factor (VEGF) is a hypoxia-induced protein that produces vascular permeability, and limited evidence suggests a possible role for VEGF in the pathophysiology of acute mountain sickness (AMS), and/or high altitude cerebral edema (HACE). Previous studies demonstrated that plasma VEGF alone does not correlate with AMS; however, soluble VEGF receptor (sFlt-1), not accounted for in previous studies, can bind VEGF in the circulation, reducing VEGF activity. In the current study, we hypothesized that free VEGF is greater and sFlt-1 less in subjects with AMS as compared to well individuals at high altitude. Methods: Subjects were exposed to 4300 m for 19-20 hours (baseline 1600 m). The incidence of AMS was determined using a modified Lake Louise symptom score and the Environmental Symptoms Questionnaire for cerebral effects. Plasma was collected at low altitude and after 24 hours at high altitude, or at time of illness, and then analyzed by ELISA for VEGF and for soluble VEGF receptor, sFlt-1. Results: AMS subjects had lower sFlt-1 at both low and high altitude as compared to well subjects, and a significant rise in free plasma VEGF on ascent to altitude compared to well subjects. Conclusion: We conclude that increased free plasma VEGF on ascent to altitude is associated with AMS, and may play a role in pathophysiology of AMS.
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