Introduction and aims: Every year, 40 million
persons travelling worldwide are at risk
of getting acute mountain sickness (AMS),
because they travel to altitudes of over
2500 m. Since asymmetric dimethylarginine
(ADMA) is a nitric oxide synthase (NOS) inhibitor,
it should increase pulmonary artery
pressure (PAP) and raise the risk of AMS and
high-altitude pulmonary edema (HAPE).
Therefore, we investigated whether changes
in ADMA levels at 4000 m can predict an individual’s
susceptibility to AMS or HAPE.
Methods: 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
related symptoms by Lake Louise Score (LLS).
Results: 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 two hours of hypoxia
we found a significant relationship between
Δ-PAPs t2 (Spearmans rho = 0.30, p ≤ 0.05) respectively
Δ-ADMA t2 (rho = –0.92, p ≤ 0.05)
and LLS.
Conclusions: After two hours of hypoxia, the
Δ-ADMA can predict an LLS of > 5 with a sensitivity
of 80 % and a specificity of 100 % and
can help assess the risk of an increase in PAP
to more than 40 mmHg (Phi coefficient: 0.69;
p ≤ 0.05).
