Naeije R, Mélot C, Lejeune P
Am Rev Respir Dis. 1986 Aug;134(2):332-3. doi: 10.1164/arrd.1986.134.2.332.
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.
在一名51岁男性身上，研究了其在海拔约5700米的厄瓜多尔钦博拉索山山顶附近登山时发生肺水肿事件前11个月以及该事件发生3周后，对急性常压吸气性低氧（吸入氧分数为0.125，其余为氮气，持续10分钟）的肺血流动力学反应。在动脉血氧分压分别降至40和43 mmHg时，肺血管阻力分别增加了72和70达因·秒·厘米⁻⁵·米²，这与先前报道的相同实验条件下正常志愿者的平均变化情况相符。这些结果表明，通过海平面低氧肺血管反应性测试无法可靠地检测出对高原肺水肿的易感性。
