Santiago T V, Neubauer J A, Edelman N H
J Appl Physiol (1985). 1986 Jan;60(1):295-8. doi: 10.1152/jappl.1986.60.1.295.
Ventilation and brain blood flow (BBF) were simultaneously measured during carbon monoxide (CO) inhalation in awake and sleeping goats up to HbCO levels of 40%. Unilateral BBF, which was continuously measured with an electromagnetic flow probe placed around the internal maxillary artery, progressively increased with CO inhalation in the awake and both sleep stages. The increase in BBF with CO inhalation during rapid-eye-movement (REM) sleep (delta BBF/delta arterial O2 saturation = 1.34 +/- 0.27 ml X min-1 X %-1) was significantly greater than that manifested during wakefulness (0.87 +/- 0.14) or slow-wave sleep (0.92 +/- 0.13). Ventilation was depressed by CO inhalation during both sleep stages but was unchanged from base-line values in awake goats. In contrast to slow-wave (non-REM) sleep, the ventilatory depression of REM sleep was primarily due to a reduction in tidal volume. Since tidal volume is more closely linked to central chemoreceptor function, we believe that these data suggest a possible role of the increased cerebral perfusion during hypoxic REM sleep. Induction of relative tissue alkalosis at the vicinity of the medullary chemoreceptor may contribute to the ventilatory depression exhibited during this sleep period.
在清醒和睡眠状态的山羊吸入一氧化碳（CO）直至HbCO水平达到40%的过程中，同时测量了通气和脑血流量（BBF）。通过放置在上颌内动脉周围的电磁流量探头连续测量单侧BBF，在清醒和两个睡眠阶段，随着CO吸入，BBF逐渐增加。在快速眼动（REM）睡眠期间，CO吸入引起的BBF增加（δBBF/δ动脉血氧饱和度=1.34±0.27 ml·min⁻¹·%-¹）显著大于清醒（0.87±0.14）或慢波睡眠（0.92±0.13）期间的增加。在两个睡眠阶段，CO吸入均会抑制通气，但清醒山羊的通气量与基线值无变化。与慢波（非REM）睡眠不同，REM睡眠期间的通气抑制主要是由于潮气量减少。由于潮气量与中枢化学感受器功能联系更为紧密，我们认为这些数据表明缺氧REM睡眠期间脑灌注增加可能发挥了作用。延髓化学感受器附近相对组织碱中毒的诱导可能导致了该睡眠期出现的通气抑制。
