A model of sleep-disordered breathing in the C57BL/6J mouse
A model of sleep-disordered breathing in the C57BL/6J mouse
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DOI：
10.1152/jappl.2001.91.6.2758
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发表时间：
2001-12-01
影响因子：
3.3
通讯作者：
O'Donnell, CP
中科院分区：
文献类型：
--
作者：
Tagaito, Y;Polotsky, VY;O'Donnell, CP
为了研究睡眠呼吸障碍（SDB）的病理生理后遗症，我们开发了一种小鼠模型，在该模型中，在睡眠期间诱导缺氧，并在唤醒或清醒时消除缺氧。在线睡眠-觉醒检测系统基于脑电图和肌电图记录的频率和幅度，用于触发睡眠期间的间歇性缺氧。在成年雄性 C57BL/6J 小鼠 (n = 5) 中，睡眠-觉醒检测系统准确评估了觉醒 (97.2 +/- 1.1%)、非快速眼动 (NREM) 睡眠 (96.0 +/- 0.9%) 和快速眼动 (REM) 睡眠 (85.6 +/- 5.0%)。连续 5 天的 SDB 后，24 小时内记录了 554 +/- 29 (SE) 次缺氧事件，发生率为 63.6 +/- 2.6 次/小时睡眠，持续时间为 28.2 +/- 0.7 秒。第 5 天吸入 O-2 分数 (FIo2) 的平均最低点为 13.2 +/- 0.1%，其中 137.1 +/- 13.2 个事件的最低点 FIo2 < 10% O-2。动脉血气证实，这种程度的缺氧会导致严重程度的低氧血症。此外，与干预后 24 小时相比，5 天的 SDB 与浅期 NREM 和 REM 睡眠的减少有关。我们的结论是，我们的 SDB 小鼠模型模拟了临床中中度至重度 SDB 患者中睡眠引起的缺氧、睡眠碎片化和总睡眠时间减少的速率和程度。
To investigate the pathophysiological sequelae of sleep-disordered breathing (SDB), we have developed a mouse model in which hypoxia was induced during periods of sleep and was removed in response to arousal or wakefulness. An on-line sleep-wake detection system, based on the frequency and amplitude of electroencephalograph and electromyograph recordings, served to trigger intermittent hypoxia during periods of sleep. In adult male C57BL/6J mice (n = 5), the sleep-wake detection system accurately assessed wakefulness (97.2 +/- 1.1%), non-rapid eye movement (NREM) sleep (96.0 +/- 0.9%) and rapid eye movement (REM) sleep (85.6 +/- 5.0%). After 5 consecutive days of SDB, 554 +/- 29 (SE) hypoxic events were recorded over a 24-h period at a rate of 63.6 +/- 2.6 events/h of sleep and with a duration of 28.2 +/- 0.7 s. The mean nadir of fraction of inspired O-2 (FIo2) on day 5 was 13.2 +/- 0.1%, and 137.1 +/- 13.2 of the events had a nadir FIo2 < 10% O-2. Arterial blood gases confirmed that hypoxia of this magnitude lead to a significant degree of hypoxemia. Furthermore, 5 days of SDB were associated with decreases in both NREM and REM sleep during the light phase compared with the 24-h postintervention period. We conclude that our murine model of SDB mimics the rate and magnitude of sleep-induced hypoxia, sleep fragmentation, and reduction in total sleep time found in patients with moderate to severe SDB in the clinical setting.