Kang J, Kimura H, Niijima M, Edo H, Sakabe H, Shinozaki T, Masuyama S, Okada O, Tatsumi K, Kuriyama T
Department of Chest Medicine, Chiba University School of Medicine, Japan.
Nihon Kyobu Shikkan Gakkai Zasshi. 1997 Nov;35(11):1173-8.
We investigated the effect of state-specific changes associated with REM sleep on pulmonary artery pressure in patients with obstructive sleep apnea (OSAS). Six male patients with OSAS (age; 40 +/- 12 SD yrs, BMI; 39.0 +/- 8.6 kg/m2, AHI; 51.5 +/- 28.5) were examined throughout the night by polysomnography, while monitoring pulmonary artery pressure via right cardiac catheterization. All patients had pulmonary hypertension (PH) during periods of wakefulness, and their mean pulmonary artery pressure (PAPm) was 31.1 +/- 7.4 mmHg. PAPm was analyzed at two different points in each apneic episode. PAPbase was the baseline value when inspiratory effects during apnea were not elicited, and PAPpeak was the peak value observed just after the cessation of OSA. PAPpeak was higher in REM (56.3 +/- 12.4) than in NREM (41.4 +/- 6.9 mmHg; P < 0.01), and both values were significantly higher than those observed during periods of wakefulness. The magnitude of elevation of PAP (delta PAP; PAPpeak-PAPbase) in REM and NREM were 11.6 +/- 2.0 and 6.9 +/- 2.8 mmHg, respectively. Relative ratios in the response of PAP to a decrease in O2 desaturation (delta PAP/delta SpO2) showed almost the same value for REM (-0.57 +/- 0.27) and NREM sleep (-0.57 +/- 0.26 mmHg/%). The values of PAPm at SpO2 75% were significantly higher in REM than in NREM (48.7 +/- 11.2 vs. 41.6 +/- 6.2 mmHg). We conclude that transient pulmonary hypertension could be caused not only by hypoxia, but also by state-specific responses (which are unrelated to hypoxia) that occur during REM sleep.
我们研究了快速眼动睡眠（REM睡眠）相关的特定状态变化对阻塞性睡眠呼吸暂停（OSAS）患者肺动脉压的影响。对6名男性OSAS患者（年龄：40±12标准差岁，体重指数：39.0±8.6kg/m²，呼吸暂停低通气指数：51.5±28.5）进行了整夜多导睡眠图检查，同时通过右心导管插入术监测肺动脉压。所有患者在清醒期均患有肺动脉高压（PH），其平均肺动脉压（PAPm）为31.1±7.4mmHg。在每个呼吸暂停发作的两个不同时间点分析PAPm。PAPbase是未引发呼吸暂停期间吸气效应时的基线值，PAPpeak是阻塞性睡眠呼吸暂停停止后立即观察到的峰值。REM睡眠期的PAPpeak（56.3±12.4）高于非快速眼动睡眠（NREM）期（41.4±6.9mmHg；P<0.01），且这两个值均显著高于清醒期观察到的值。REM睡眠期和NREM睡眠期肺动脉压升高幅度（ΔPAP；PAPpeak - PAPbase）分别为11.6±2.0和6.9±2.8mmHg。肺动脉压对氧饱和度降低的反应相对比值（ΔPAP/ΔSpO2）在REM睡眠期（-0.57±0.27）和NREM睡眠期（-0.57±0.26mmHg/%）几乎相同。血氧饱和度为75%时的PAPm值在REM睡眠期显著高于NREM睡眠期（48.7±11.2对41.6±6.2mmHg）。我们得出结论，短暂性肺动脉高压不仅可能由缺氧引起，还可能由REM睡眠期间发生的特定状态反应（与缺氧无关）引起。
