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对１４例慢性高山病（ＣＭＳ）患者的低氧肺泡通气不足的发病机理和肺功能作了研究。与对照组比较，ＣＭＳ组的Ｐ＿（ＥＴ）ｃｏ＿２高，ＶＴ低，低氧通气反应（ＨＶＲ）Ａ值低；吸入高浓度Ｏ＿２后，ＣＭＳ组的Ｖ＿Ｅ显著增加。提示ＣＭＳ组存在ＨＶＲ降低和中枢性低氧通气抑制。静注纳洛酮不能逆转已降低的ＨＶＲ。ＣＭＳ的ＦＥＶ＿１／ＶＣ比值降低并加重动脉低氧血症。结果表明：周围性ＨＶＲ降低和中枢性低氧通气抑制是引起高原低氧肺泡通气不足的因素。而肺泡通气不足与阻塞性肺疾病是导致ＣＭＳ发生的主要原因。
The pathogenesis and pulmonary function of hypoxic alveolar hypoventilation in 14 patients with chronic mountain sickness (CMS) were studied. Compared with the control group, the P_ (ET) co_2 of CMS group was high, the VT was low, and the value of A was lower in hypoxia ventilation (HVR). The V_E of CMS group was significantly increased after inhaling high concentration of O_2. It suggested that there was HVR reduction and central hypoxia-inhibition in CMS group. Intravenous naloxone does not reverse already reduced HVR. CMS decreased FEV 1 / VC ratio and aggravated arterial hypoxemia. The results showed that the reduction of peripheral HVR and central hypoxia was the cause of hypoxia-alveolar hypoventilation in plateau. Alveolar hypoventilation and obstructive pulmonary disease are the main causes of CMS.