Oxidative Stress in Hypobaric Hypoxia

Background

Altitude related illness, which include acute mountain sickness (AMS), high altitude pulmonary edema (HAPE) and high altitude cerebral edema (HACE), is common in subjects exposed to high altitude during professional or leisure time activities. There are independent risk factors such as: individual susceptibility and rate of ascent. HAPE is a potentially life-threatening complication of high altitude stay, mostly occuring within the first 2-5 days of exposure. Although there is a controversial discussion, excessive hypoxic pulmonary vasoconstriction is thought to be the main trigger for developing HAPE. Beside the controversial discussion if hypobaric hypoxia leads to oxidative stress it is not known whether oxidative stress contributes to AMS or HAPE.

Objective

The investigators hypothesize that reactive oxygen species are generated during high altitude stay and contribute to the development of acute mountain sickness. Furthermore they would like to describe other changes in metabolic pathways possibly contributing to vessel tone dysregulation.

Methods

36 healthy volunteers will examined during an high altitude medical research expedition to Mount Muztagh ata (7549m) in Western China. Acute mountain sickness scores and clinical parameters will be assessed. Metabolomics analysis of more than 390 parameters, using a mass spectrometry-based targeted metabolomic platform, is used to detect systemic oxidative stress and functional impairment of enzymes that require oxidation-sensitive co-factors. Furthermore routine laboratory test will be done, for example CRP, creatinine and interleukines

Inclusion criteria

• healthy
• physical fit
• mountaineering experience
• 18-70 years

Exclusion criteria

• any type of disease
• regular intake of medicaments
• history of high altitude pulmonary edema
• severe acute mountain sickness below an altitude of 3500m
• any history of high altitude cerebral edema