da Silva Sérgio P, Hulce Verne D, Backs Richard W
Central Michigan University, Mount Pleasant, USA.
Sleep Breath. 2009 May;13(2):147-56. doi: 10.1007/s11325-008-0228-0. Epub 2008 Oct 24.
The present study investigated whether autonomic control of the heart for persons with low and high levels of sleep apnea/hypopnea differed between sleep stages and across the sleep period.
Electrocardiography and impedance cardiography of 24 patients referred to polysomnography were recorded through the night. A mixed repeated-measures and between-subjects, quasi-experimental design was utilized. Heart period, high frequency heart rate variability, and pre-ejection period were computed, respectively, as measure of heart rate and estimates of parasympathetic and sympathetic control. The cardiac and autonomic measures for participants with low apnea-hypopnea indices were compared to those of patients with high rates of apnea-hypopnea across the sleep period and sleep stages. Cardiac rates of the two groups decreased incrementally through the sleep period. Cardiovascular measures during sleep from the group with high rates of apnea-hypopnea indicated larger parasympathetic activation in relation to wake baseline for epochs without arousals than from the group with low apnea-hypopnea rates. Parasympathetic activation during nonrapid-eye movement (non-REM) sleep (sleep stage 2) was significantly greater than during REM sleep. Higher levels of apnea-hypopnea seem to be associated with increased parasympathetic control, especially during lighter, non-REM sleep. A possible explanation for this phenomenon is a compensatory response to oxygen desaturation caused by disturbed breathing.
本研究调查了睡眠呼吸暂停/低通气水平低和高的人群心脏的自主控制在睡眠阶段之间以及整个睡眠期间是否存在差异。
对24名接受多导睡眠监测的患者进行了整夜的心电图和阻抗心动图记录。采用了混合重复测量和被试间的准实验设计。分别计算了心动周期、高频心率变异性和射血前期，作为心率的测量指标以及副交感神经和交感神经控制的估计值。将呼吸暂停低通气指数低的参与者与呼吸暂停低通气率高的患者在整个睡眠期间和睡眠阶段的心脏和自主神经测量指标进行了比较。两组的心率在整个睡眠期间逐渐下降。呼吸暂停低通气率高的组在无觉醒的睡眠期间相对于清醒基线显示出更大的副交感神经激活，比呼吸暂停低通气率低的组更明显。非快速眼动（非REM）睡眠（睡眠阶段2）期间的副交感神经激活明显大于快速眼动睡眠期间。较高水平的呼吸暂停低通气似乎与副交感神经控制增加有关，尤其是在较浅的非快速眼动睡眠期间。对这一现象的一种可能解释是对呼吸紊乱导致的氧饱和度下降的一种代偿反应。
