反复觉醒对心血管系统的影响：探究OSAHS患者心血管并发症的发生机制
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摘要
目标：本研究旨在探究反复觉醒对健康受试者心血管系统的影响,从而明确这一病理生理过程在阻塞性睡眠呼吸暂停综合征患者心血管并发症发生过程中的地位。
方法：20名青年男性健康受试者(年龄25.0±2.1岁,BMI22.9±1.9kg·m2),在睡眠实验室接受连续两夜多导睡眠图监测。第一夜为基础对照夜,不对受试者进行任何干预；第二夜为刺激实验夜,应用音频信号对受试者进行反复刺激以诱发觉醒,此种音频信号刺激持续整个睡眠过程,期望达到的觉醒指数(arousal index, ArI)为60次/小时。比较两夜的睡眠结构、主观睡眠质量、血压、心率变异率、动脉硬度指数以及特定血清学指标。睡眠结构指标包括总睡眠时间,N1、N2、N3、REM各期睡眠时间及比例以及Arl。St Mary's医院睡眠问卷用于对睡眠质量及连续性进行主观评价。分别在对照夜睡前(C1)、醒后(C2),实验夜睡前(T1)、醒后(T2)测量血压,并记录清醒平静仰卧状态下的心电图及指端血流量脉搏(digital volume pulse, DVP)。用快速傅立叶变换进行心率变异率分析,得到上述四个时间点的标准化低频功率(low frequency power in normalized unit, LF),标准化高频功率(high frequency power in normalized unit, HF)以及低频-高频功率之比(LF/HF ratio, LHR),并以此来评价自主神经系统状态；对指端血流量脉搏波形进行分析,得到上述四个时间点的动脉硬度指数(stiffness index, SI)。比较上述血压、心率变异率指标以及硬度指数在对照夜和实验夜的改变量有无显著性差异(即T2-T1与C2-C1是否有差别),若有则进一步分析这些指标各自在对照夜前后及实验夜前后发生了何种变化。测定血清中CRP、IL-6, TNF-α、VEGF、NO、ET-1的浓度,比较两日之间有无显著性差异。Spearman相关分析用于分析上述指标间的相关性。
结果：实验夜实际达到的觉醒指数为44±9(27-55.2)次/小时。在各项睡眠结构指标中,两夜相比其差异具有统计学意义的为实验夜N3期睡眠时间显著短于对照夜(P=0.039)；实验夜ArI显著高于对照夜(P<0.001)。就“醒后头脑清醒程度”而言,受试者认为实验夜不如对照夜(P=0.019),实验夜受试者能意识到的觉醒次数显著多于对照夜(P<0.001)。实验夜醒后舒张压显著高于睡前(P=0.003),且升高的程度与对照夜相比具有统计学意义(P=0.026)；两夜舒张压改变量的差值与两夜N2睡眠比例的差值具有线性相关关系(P=0.011)。实验夜醒后LF和LHR显著高于睡前(P<0.001),HF显著低于睡前(P<0.001),这些变化的程度与对照夜相比具有统计学意义(均有P<0.001)；实验夜HF的改变与REM睡眠时间及比例具有线性相关关系(P=0.003,P=0.006)；实验夜LHR的改变同样与REM睡眠时间及比例具有线性相关关系(P=0.008,P=0.027)。SI在两夜的改变量无明显差别。CRP、IL-6, TNF-α、VEGF、NO、ET-1等血清学指标两次测量结果无显著性差异。
结论：利用音频信号刺激诱发反复觉醒以模拟OSAHS中出现的反复觉醒可引起交感神经活性升高,副交感神经活性下降,且这种改变在觉醒停止后一段时间仍然存在,提示其效应具有可累积性。反复觉醒导致晨起舒张压增高,可能与睡眠结构的改变有关,但意义尚不明确。在OSAHS相关的心血管疾病的发生过程中,自主神经系统状态的改变有可能是早于血管内皮功能紊乱的病理生理过程。
Objectives:To investigate whether repetitive arousals will lead to overt changes in cardiovascular system in healthy subjects. To give clues to the understanding of the pathophysiology of cardiovascular diseases secondary to obstructive sleep apnea hypopnea syndrome (OSAHS) and the roles that repetitive arousals play in it.
Methods:Polysomnography was conducted on two consecutive nights for twenty healthy young male subjects (age25.0±2.1, BMI22.9±1.9kg·m-2). The first night functioned as a baseline-control and was free of any intervention. On the second night, arousals were repeatedly induced by auditory stimuli applied repetitively over the whole night and the resulted arousal index (ArI) was expected to be60hr-1at the best. Sleep architecture, subjective assessment of sleep quality, blood pressure, heart rate variability (HRV) variables, arterial stiffness index and certain serum markers were compared between the two nights. Parameters of sleep architecture include total sleep time, ArI and the time spent in and the percentages of N1, N2, N3and REM sleep. St Mary's hospital sleep questionnaire was used to evaluate the quality and continuity of sleep subjectively. Blood pressure (BP) was measured, and electrocardiography and digital volume pulse (DVP) were recorded under undisturbed conditions while subjects were awake on the following four occasions respectively, before lights-off on control night (C1), after lights-on on control night (C2), before lights-off on test night (T1), and after lights-on on test night (T2). HRV analysis was carried out applying the fast Fourier transform method and low frequency power in normalized unit (LF), high frequency power in normalized unit (HF) and LF/HF ratio (LHR) were deduced to assess the status of autonomic nervous system. Stiffness index (SI) was calculated from the contour analysis of digital volume pulse. To study the effects on BP, SI and HRV indices of the intervention, we compared the change in each of these variables over the test night (T2-T1) to the change over the control night (C2-C1). If the difference between these two changes was significant, we further compared T2to Tl and C2to Cl respectively to find out what changes occurred. CRP, IL-6, TNF-α, VEGF, NO, ET-1in serum were measured and compared between the two nights. Correlation was explored with the Spearman method.
Results:The ArI on test night was actually44±9(27-55.2) hr-1. The time spent in N3 sleep on test night was significantly less than that on control night (P=0.039) and the Arl on test night was no surprisingly much higher than that on control night (P<0.001). When asked about the alertness upon awakening in the morning, subjects confessed that it was worse following the test night (P=0.019). Subjectively, they reported more arousals for the test night as compared to control night (P<0.001). The post-sleep diastolic blood pressure (DBP) was higher than the pre-sleep one for the test night (P=0.003) and the increment was remarkable when compared with the control night (P=0.026). The difference between the change in DBP over the test night and that over the control night was correlated with the difference in the percentages of N2sleep on the two nights (P=0.011). Regarding to the HRV indices, LF and LHR increased throughout the test night while HF decreased (all P<0.001). When compared with control night, all the changes over the test night were statistically significant (all P<0.001). The change in HF over the test night was correlated with the time spent in and percentage of REM sleep on the same night (P=0.003, P=0.006). The change in LHR over the test night was correlated with the same sleep indices with P value of0.008and0.027respectively. The changes in SI over the two nights were not significantly different from each other. None of the changes in any of the biomarkers between the two nights reached the significance.
Conclusions:We demonstrate that exposure to repetitive arousals induced by auditory stimuli leads to elevation of sympathetic nervous system activity and reduction of parasympathetic nervous system activity, which remain evident after the arousals end for a while, indicating the cumulative effect of repetitive arousals on autonomic nervous system. Repetitive arousals also cause an increase of diastolic blood pressure in the morning which might be related to the disturbance to sleep architecture, but the underlying mechanisms has not been fully elucidated yet. Considering no obvious changes have been discovered in stiffness index or biomarkers, it is very likely that the shift in sympatho-vagal balance occurs prior to endothelial dysfunction in the development of cardiovascular disease in OSAHS patients.
方法：20名青年男性健康受试者(年龄25.0±2.1岁,BMI22.9±1.9kg·m2),在睡眠实验室接受连续两夜多导睡眠图监测。第一夜为基础对照夜,不对受试者进行任何干预；第二夜为刺激实验夜,应用音频信号对受试者进行反复刺激以诱发觉醒,此种音频信号刺激持续整个睡眠过程,期望达到的觉醒指数(arousal index, ArI)为60次/小时。比较两夜的睡眠结构、主观睡眠质量、血压、心率变异率、动脉硬度指数以及特定血清学指标。睡眠结构指标包括总睡眠时间,N1、N2、N3、REM各期睡眠时间及比例以及Arl。St Mary's医院睡眠问卷用于对睡眠质量及连续性进行主观评价。分别在对照夜睡前(C1)、醒后(C2),实验夜睡前(T1)、醒后(T2)测量血压,并记录清醒平静仰卧状态下的心电图及指端血流量脉搏(digital volume pulse, DVP)。用快速傅立叶变换进行心率变异率分析,得到上述四个时间点的标准化低频功率(low frequency power in normalized unit, LF),标准化高频功率(high frequency power in normalized unit, HF)以及低频-高频功率之比(LF/HF ratio, LHR),并以此来评价自主神经系统状态；对指端血流量脉搏波形进行分析,得到上述四个时间点的动脉硬度指数(stiffness index, SI)。比较上述血压、心率变异率指标以及硬度指数在对照夜和实验夜的改变量有无显著性差异(即T2-T1与C2-C1是否有差别),若有则进一步分析这些指标各自在对照夜前后及实验夜前后发生了何种变化。测定血清中CRP、IL-6, TNF-α、VEGF、NO、ET-1的浓度,比较两日之间有无显著性差异。Spearman相关分析用于分析上述指标间的相关性。
结果：实验夜实际达到的觉醒指数为44±9(27-55.2)次/小时。在各项睡眠结构指标中,两夜相比其差异具有统计学意义的为实验夜N3期睡眠时间显著短于对照夜(P=0.039)；实验夜ArI显著高于对照夜(P<0.001)。就“醒后头脑清醒程度”而言,受试者认为实验夜不如对照夜(P=0.019),实验夜受试者能意识到的觉醒次数显著多于对照夜(P<0.001)。实验夜醒后舒张压显著高于睡前(P=0.003),且升高的程度与对照夜相比具有统计学意义(P=0.026)；两夜舒张压改变量的差值与两夜N2睡眠比例的差值具有线性相关关系(P=0.011)。实验夜醒后LF和LHR显著高于睡前(P<0.001),HF显著低于睡前(P<0.001),这些变化的程度与对照夜相比具有统计学意义(均有P<0.001)；实验夜HF的改变与REM睡眠时间及比例具有线性相关关系(P=0.003,P=0.006)；实验夜LHR的改变同样与REM睡眠时间及比例具有线性相关关系(P=0.008,P=0.027)。SI在两夜的改变量无明显差别。CRP、IL-6, TNF-α、VEGF、NO、ET-1等血清学指标两次测量结果无显著性差异。
结论：利用音频信号刺激诱发反复觉醒以模拟OSAHS中出现的反复觉醒可引起交感神经活性升高,副交感神经活性下降,且这种改变在觉醒停止后一段时间仍然存在,提示其效应具有可累积性。反复觉醒导致晨起舒张压增高,可能与睡眠结构的改变有关,但意义尚不明确。在OSAHS相关的心血管疾病的发生过程中,自主神经系统状态的改变有可能是早于血管内皮功能紊乱的病理生理过程。
Objectives:To investigate whether repetitive arousals will lead to overt changes in cardiovascular system in healthy subjects. To give clues to the understanding of the pathophysiology of cardiovascular diseases secondary to obstructive sleep apnea hypopnea syndrome (OSAHS) and the roles that repetitive arousals play in it.
Methods:Polysomnography was conducted on two consecutive nights for twenty healthy young male subjects (age25.0±2.1, BMI22.9±1.9kg·m-2). The first night functioned as a baseline-control and was free of any intervention. On the second night, arousals were repeatedly induced by auditory stimuli applied repetitively over the whole night and the resulted arousal index (ArI) was expected to be60hr-1at the best. Sleep architecture, subjective assessment of sleep quality, blood pressure, heart rate variability (HRV) variables, arterial stiffness index and certain serum markers were compared between the two nights. Parameters of sleep architecture include total sleep time, ArI and the time spent in and the percentages of N1, N2, N3and REM sleep. St Mary's hospital sleep questionnaire was used to evaluate the quality and continuity of sleep subjectively. Blood pressure (BP) was measured, and electrocardiography and digital volume pulse (DVP) were recorded under undisturbed conditions while subjects were awake on the following four occasions respectively, before lights-off on control night (C1), after lights-on on control night (C2), before lights-off on test night (T1), and after lights-on on test night (T2). HRV analysis was carried out applying the fast Fourier transform method and low frequency power in normalized unit (LF), high frequency power in normalized unit (HF) and LF/HF ratio (LHR) were deduced to assess the status of autonomic nervous system. Stiffness index (SI) was calculated from the contour analysis of digital volume pulse. To study the effects on BP, SI and HRV indices of the intervention, we compared the change in each of these variables over the test night (T2-T1) to the change over the control night (C2-C1). If the difference between these two changes was significant, we further compared T2to Tl and C2to Cl respectively to find out what changes occurred. CRP, IL-6, TNF-α, VEGF, NO, ET-1in serum were measured and compared between the two nights. Correlation was explored with the Spearman method.
Results:The ArI on test night was actually44±9(27-55.2) hr-1. The time spent in N3 sleep on test night was significantly less than that on control night (P=0.039) and the Arl on test night was no surprisingly much higher than that on control night (P<0.001). When asked about the alertness upon awakening in the morning, subjects confessed that it was worse following the test night (P=0.019). Subjectively, they reported more arousals for the test night as compared to control night (P<0.001). The post-sleep diastolic blood pressure (DBP) was higher than the pre-sleep one for the test night (P=0.003) and the increment was remarkable when compared with the control night (P=0.026). The difference between the change in DBP over the test night and that over the control night was correlated with the difference in the percentages of N2sleep on the two nights (P=0.011). Regarding to the HRV indices, LF and LHR increased throughout the test night while HF decreased (all P<0.001). When compared with control night, all the changes over the test night were statistically significant (all P<0.001). The change in HF over the test night was correlated with the time spent in and percentage of REM sleep on the same night (P=0.003, P=0.006). The change in LHR over the test night was correlated with the same sleep indices with P value of0.008and0.027respectively. The changes in SI over the two nights were not significantly different from each other. None of the changes in any of the biomarkers between the two nights reached the significance.
Conclusions:We demonstrate that exposure to repetitive arousals induced by auditory stimuli leads to elevation of sympathetic nervous system activity and reduction of parasympathetic nervous system activity, which remain evident after the arousals end for a while, indicating the cumulative effect of repetitive arousals on autonomic nervous system. Repetitive arousals also cause an increase of diastolic blood pressure in the morning which might be related to the disturbance to sleep architecture, but the underlying mechanisms has not been fully elucidated yet. Considering no obvious changes have been discovered in stiffness index or biomarkers, it is very likely that the shift in sympatho-vagal balance occurs prior to endothelial dysfunction in the development of cardiovascular disease in OSAHS patients.
引文
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