Trinder John, Ivens Clare, Kleiman Jan, Kleverlaan Darci, White David P
Department of Psychology, University of Melbourne, Parkville, Vic. 3010, Australia.
J Sleep Res. 2006 Jun;15(2):174-82. doi: 10.1111/j.1365-2869.2006.00513.x.
Arousal from sleep is associated with transient cardiorespiratory activation. Traditionally, this response has been understood to be a consequence of state-dependent changes in the homeostatic control of ventilation. The hypothesis predicts that the magnitude of ventilatory and cardiac responses at an arousal will be a function of the intensity of concurrent respiratory stimuli (primarily PCO(2)). Alternatively, it has been proposed that increased cardiorespiratory activity is due to reflex activation. This hypothesis predicts that the magnitude of the cardiorespiratory response will be independent of respiratory stimuli. To compare these hypotheses we measured minute ventilation (V(i)), heart rate (HR) and blood pressure (BP) during wakefulness and stage 2 sleep, while manipulating P(et)CO(2). Further, we assessed the magnitude of the response of these variables to an arousal from sleep at the various levels of P(et)CO(2). The subjects were male aged 18-25 years. P(et)CO(2) was manipulated by clamping it at four levels during wakefulness [wake eucapnic, sleep eucapnic (Low), and sleep eucapnic +3 mmHg (Medium) and +6 mmHg (High)] and three levels during sleep (Low, Medium and High). The average number of determinations for each subject at each level was 14 during wakefulness and 25 during sleep. Arousals were required to meet American Sleep Disorders Association criteria and were without body movement. The results indicated that average increases in V(i), HR and BP at arousal from sleep did not significantly differ as a function of the level of P(et)CO(2) present at the time of the arousal (all P > 0.05). Further, the magnitude of the ventilatory response to an arousal was significantly less than the values predicted by the homeostatic hypothesis (P < 0.05). We conclude that, in normal subjects, the cardiorespiratory response to an arousal from sleep is not because of a homeostatic response, but of a reflex activation.
从睡眠中觉醒与短暂的心肺激活有关。传统上，这种反应被理解为通气稳态控制中状态依赖性变化的结果。该假设预测，觉醒时通气和心脏反应的幅度将是同时存在的呼吸刺激强度（主要是PCO₂）的函数。另外，有人提出心肺活动增加是由于反射激活。该假设预测心肺反应的幅度将与呼吸刺激无关。为了比较这些假设，我们在清醒和睡眠2期测量了分钟通气量（V̇ₑ）、心率（HR）和血压（BP），同时控制呼气末二氧化碳分压（P̅ₑₜCO₂）。此外，我们评估了在不同P̅ₑₜCO₂水平下这些变量对睡眠觉醒反应的幅度。受试者为18至25岁的男性。通过在清醒时将P̅ₑₜCO₂钳定在四个水平[清醒时呼气末二氧化碳正常、睡眠时呼气末二氧化碳正常（低）、睡眠时呼气末二氧化碳正常+3 mmHg（中）和+6 mmHg（高）]以及在睡眠时钳定在三个水平（低、中、高）来控制P̅ₑₜCO₂。每个受试者在每个水平的平均测定次数在清醒时为14次，在睡眠时为25次。觉醒需符合美国睡眠障碍协会的标准且无身体运动。结果表明，睡眠觉醒时V̇ₑ、HR和BP的平均增加量并未因觉醒时存在的P̅ₑₜCO₂水平而有显著差异（所有P>0.05）。此外，觉醒时通气反应的幅度明显小于稳态假设预测的值（P<0.05）。我们得出结论，在正常受试者中，睡眠觉醒时的心肺反应不是由于稳态反应，而是由于反射激活。
