[9] At 4559 m, inhalation of NO led to a marked decrease in PAP and an increase in arterial oxygen saturation especially in subjects susceptible to HAPE.[10] In addition, decreased pulmonary NO production during acute hypoxia was suggested to contribute among other learn more factors to the enhanced hypoxic pulmonary vascular response in HAPE-susceptible subjects[11] and therefore might contribute to exaggerated hypoxic pulmonary vasoconstriction and in turn to pulmonary edema.[12] As

it is an NOS inhibitor, ADMA should cause an increase in PAP and raise the risk of developing altitude sickness and HAPE. By measuring ADMA serum levels during standardized altitude exposure, we were able to assess this approach both from a principal therapeutic perspective as described in the aforementioned studies and from a diagnostic perspective. This prospective comparative study was conducted to test the hypothesis that there is a relationship between Δ-ADMA in blood and a hypoxia-induced increase in PAP and AMS and that ADMA could be a predictive value for the development of AMS or a PAP > 40 mmHg. The tests

were performed in the altitude and climate chamber of the German Air Force Institute of Aviation Medicine in Koenigsbrueck, Germany (134 m). This hypobaric EGFR activation chamber has a capacity of six individuals for an overnight stay. Two tests were performed and 12 subjects could be investigated. Each trial consisted of two overnight stays in the chamber. The subjects were allowed to sleep. For intraindividual comparison, both nights followed the same protocol. Altitude conditions, however, were simulated only during the second night, when the

subjects were decompressed over a period of 53 minutes to a pressure equivalent to an altitude second of 4000 m. The subjects spent 12 hours in the chamber under these altitude conditions. At all time points, the subjects could have been rapidly recompressed or could have left the chamber through an airlock. An emergency physician with expertise in altitude medicine was continuously present. The study design had been approved by the ethics committee of the Society of Physicians of the state of Baden-Wuerttemberg, Stuttgart, Germany. All participants had given their written informed consent to take part in the study. Twelve male subjects (median age: 23 years, range: 18–33 years; median height: 182.5 cm, range: 169–194 cm; median weight: 76 kg, range: 55–100 kg; median body mass index: 22.5 kg/m2, range: 19–29 kg/m2) without altitude exposure higher than 1500 m in the last month prior to this study showed a minor tricuspid valve insufficiency found incidentally in the context of this study and were otherwise healthy. Prior to the tests, the subjects received an echocardiogram (ECG). Blood tests (HBG, HCT, RBC, MCH, MCV, PLT) and a 12-channel ECG were performed immediately before the trial. All results were unremarkable.