Sforza Emilia, Chapotot Florian, Lavoie Suzie, Roche Frederic, Pigeau Ross, Buguet Alain
Service de Psychiatrie Adulte, Laboratoire de Sommeil, Hôpitaux Universitaires de Genève, 2 Chemin du Petit Bel Air, 1225 Chêne Bourg, Geneva, Switzerland.
Clin Neurophysiol. 2004 Nov;115(11):2442-51. doi: 10.1016/j.clinph.2004.06.002.
Arousal (AR) from sleep is associated with an autonomic reflex activation raising blood pressure and heart rate (HR). Recent studies indicate that sleep deprivation may affect the autonomic system, contributing to high vascular risk. Since in sleep disorders a sleep fragmentation and a partial sleep deprivation occurs, it could be suggested that the cardiovascular effects observed at AR from sleep might be physiologically affected when associated with sleep deprivation. The aim of the study was to examine the effect of sleep deprivation on cardiac arousal response in healthy subjects.
Seven healthy male subjects participated in a 64 h sleep deprivation protocol. Arousals were classified into four groups, i.e. >3<6 s, >6<10 s, >10<15 s and >15 s, according to their duration. Pre-AR HR values were measured during 10 beats preceding the AR onset, and the event-related HR fluctuations were calculated during the 20 beats following AR onset. As an index of cardiac activation, the ratio of highest HR in the post-AR period over the lowest recorded before AR (HR ratio) was calculated.
For AR lasting less than 10 s, the occurrence of AR induces typical HR oscillations in a bimodal pattern, tachycardia followed by bradycardia. For AR lasting more than 10 s, i.e. awakenings, the pattern was unimodal with a more marked and sustained HR rise. The HR response was consistently similar across nights, during NREM and REM sleep, without difference between conditions.
Overall, total sleep deprivation appeared to have no substantial effect on cardiac response to spontaneous arousals and awakenings from sleep in healthy subjects. Further studies are needed to clarify the role of chronic sleep deprivation on cardiovascular risk in patients with sleep disorders.
In healthy subjects acute prolonged sleep deprivation does not affect the cardiac response to arousal.
睡眠中的觉醒（AR）与自主神经反射激活相关，会导致血压和心率（HR）升高。近期研究表明，睡眠剥夺可能会影响自主神经系统，增加血管疾病风险。由于睡眠障碍会导致睡眠片段化和部分睡眠剥夺，因此可以推测，睡眠中的觉醒所观察到的心血管效应在与睡眠剥夺相关时可能会受到生理影响。本研究的目的是检验睡眠剥夺对健康受试者心脏觉醒反应的影响。
7名健康男性受试者参与了一项64小时的睡眠剥夺方案。根据觉醒的持续时间，将其分为四组，即>3<6秒、>6<10秒、>10<15秒和>15秒。在觉醒发作前的10次心跳期间测量觉醒前的心率值，并在觉醒发作后的20次心跳期间计算与事件相关的心率波动。作为心脏激活的指标，计算觉醒后时期的最高心率与觉醒前记录的最低心率之比（心率比）。
对于持续时间小于10秒的觉醒，觉醒的发生会诱发典型的双峰模式心率振荡，先是心动过速，随后是心动过缓。对于持续时间超过10秒的觉醒，即觉醒状态，模式为单峰，心率上升更明显且持续时间更长。在整个夜间、非快速眼动睡眠和快速眼动睡眠期间，心率反应始终相似，不同条件之间无差异。
总体而言，完全睡眠剥夺似乎对健康受试者睡眠中自发觉醒和觉醒时的心脏反应没有实质性影响。需要进一步研究以阐明慢性睡眠剥夺在睡眠障碍患者心血管风险中的作用。
在健康受试者中，急性长期睡眠剥夺不会影响对觉醒的心脏反应。
