Hackett P H, Roach R C, Schoene R B, Harrison G L, Mills W J
Denali Medical Research Project, Center for High Latitude Health Research, University of Alaska, Anchorage 99508.
J Appl Physiol (1985). 1988 Mar;64(3):1268-72. doi: 10.1152/jappl.1988.64.3.1268.
We wished to determine the role of hypoxic chemosensitivity in high-altitude pulmonary edema (HAPE) by studying persons when ill and upon recovery. We studied seven males with HAPE and seventeen controls at 4,400 m on Mt. McKinley. We measured ventilatory responses to both O2 breathing and progressive poikilocapnic hypoxia. Hypoxic ventilatory response (HVR) was described by the slope relating minute ventilation to percent arterial O2 saturation (delta VE/delta SaO2%). HAPE subjects were quite hypoxemic (SaO2% 59 +/- 6 vs. 85 +/- 1, P less than 0.01) and showed a high-frequency, low-tidal-volume pattern of breathing. O2 decreased ventilation in controls (-20%, P less than 0.01) but not in HAPE subjects. The HAPE group had low HVR values (0.15 +/- 0.07 vs. 0.54 +/- 0.08, P less than 0.01), although six controls had values in the same range. The three HAPE subjects with the lowest HVR values were the most hypoxemic and had a paradoxical increase in ventilation when breathing O2. We conclude that a low HVR plays a permissive rather than causative role in the pathogenesis of HAPE and that the combination of extreme hypoxemia and low HVR may result in hypoxic depression of ventilation.
我们希望通过对患病人员及其康复后的研究来确定低氧化学敏感性在高原肺水肿（HAPE）中的作用。我们在麦金利山海拔4400米处研究了7名患HAPE的男性和17名对照者。我们测量了对吸氧和进行性变温性低氧的通气反应。低氧通气反应（HVR）通过分钟通气量与动脉血氧饱和度百分比之间的斜率（δVE/δSaO2%）来描述。HAPE受试者严重低氧（SaO2%为59±6，而对照组为85±1，P<0.01），并表现出高频、低潮气量的呼吸模式。吸氧使对照组的通气量降低（-20%，P<0.01），但对HAPE受试者无效。HAPE组的HVR值较低（0.15±0.07，而对照组为0.54±0.08，P<0.01），尽管有6名对照者的值在同一范围内。HVR值最低的3名HAPE受试者低氧最为严重，且在吸氧时通气量出现反常增加。我们得出结论，低HVR在HAPE发病机制中起允许作用而非致病作用，极端低氧和低HVR的组合可能导致通气的低氧抑制。
