With this in mind, we investigated whether changes in ADMA levels (Δ-ADMA) at an altitude of 4000 m can predict an individual’s susceptibility to AMS or HAPE. Twelve subjects spent two nights in a hypobaric chamber, the first night without exposure to altitude conditions and the second night at a simulated altitude of 4000 m. At identical

time points during both nights (after 2, 5, and 11 hours), we determined ADMA serum levels, PAP by Doppler echocardiography and estimated hypoxia c-Met inhibitor related symptoms by Lake Louise Score (LLS). Contrary to our initial hypothesis, subjects with a marked increase in ADMA at 4000 m showed PAP levels below the critical threshold for HAPE and were not affected by AMS. By contrast, subjects with a decrease in ADMA suffered from AMS and had PAP levels above 40 mmHg. After 2 hours of hypoxia we found a significant relationship between Δ-PAP t2 (Spearmans ρ = 0.30, p ≤ 0.05) respectively Δ-ADMA t2 (ρ = −0.92, p ≤ 0.05) and LLS. After 2 hours of hypoxia, the Δ-ADMA (positive or negative) can predict an LLS of >5 with a sensitivity of 80% and a specificity of 100% and can help assess

LBH589 research buy the risk of an increase in PAP to more than 40 mmHg and thus the risk of HAPE (ϕ coefficient: 0.69; p ≤ 0.05). Worldwide, 40 million tourists are at risk of getting acute mountain sickness (AMS) each year, because they travel to altitudes of higher than 2500 m (AMS-incidence at altitudes of 2500–3000

m: 10–30%).[1-4] In general, the following conditions are distinguished: AMS, high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). An increase in pulmonary artery pressure (PAP), which is subject to individual differences, plays a crucial role in the development of HAPE.[5] The risk of developing HAPE increases massively when PAP exceeds 40 mmHg.[6] The measurement of PAP by Doppler echocardiography usually allows individuals at Ureohydrolase risk of developing HAPE to be identified, especially in the setting of hypoxia.[7] For methodological reasons, however, Doppler echocardiography can be used only in individuals with (at least minor) tricuspid valve insufficiency. Although this insufficiency is often seen in association with an altitude-induced increase in PAP, high-altitude medical research has revealed the absence of tricuspid reflux in 5–30% of the subjects.[8] In addition, this method requires an experienced examiner and the availability of a suitable (mobile) system. This explains the need for simpler procedures. Against this background, the measurement of serum levels of asymmetric dimethylarginine (ADMA) may provide a new diagnostic approach. ADMA is a potent inhibitor of nitric oxide synthase (NOS). By increasing cyclic guanosine monophosphate (cGMP), nitric oxide (NO) causes smooth muscle relaxation and therefore induces rapid vasodilatation.