The pulmonary hemodynamic response to an acute normobaric inspiratory hypoxia, a fraction of inspired O2 of 0.125 and the balance nitrogen for 10 min, was investigated in a 51-year-old man 11 months before and again 3 wk after he experienced an episode of pulmonary edema while mountaineering near the summit of the Chimborazo (Ecuador) at an altitude of about 5,700 m. Pulmonary vascular resistance increased by 72 and 70 dyne . s . cm-5 . m2 in the presence of decreased arterial PO2 to 40 and 43 mmHg, respectively, which is in the average of previously reported changes in normal volunteers in identical experimental conditions. These results suggest that susceptibility to high altitude pulmonary edema cannot be reliably detected by pulmonary vasoreactivity testing to hypoxia at sea level.