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
发布时间：2018-07-15 08:10
【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(P0.001)。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(P0.001)。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(P0.001),HF显著低于睡前(P0.001),这些变化的程度与对照夜相比具有统计学意义(均有P0.001)；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。
[Abstract]:Objective: This study aims to explore the effect of repeated awakening on the cardiovascular system of healthy subjects, and to identify the status of this pathophysiological process in the process of cardiovascular complications in patients with obstructive sleep apnea syndrome.
Methods: 20 young male healthy subjects (age 25 + 2.1 years old, BMI22.9 + 1.9kg m2) were monitored in the sleep laboratory for two night polysomnography. The first night was the basis control night, and no intervention was done on the subjects. Second night was used to stimulate the experimental night, and the subjects were repeatedly stimulated with audio signals to induce awakening, An audio signal stimulates the whole sleep process. The desired awakening index (arousal index, ArI) is expected to be 60 times per hour. The sleep structure of two nights, subjective sleep quality, blood pressure, heart rate variability, arterial hardness index, and specific serological indexes. Sleep structure indexes including total sleep time, N1, N2, N3, REM, and REM periods are also compared. The ratio and the Arl.St Mary's Hospital Sleep Questionnaire were used to evaluate the quality and continuity of sleep. In the control night before night (C1), after waking up (C2), at night before sleep (T1), after waking up (T2), the blood pressure was measured and the blood flow pulse (Digital volume pulse, DVP) was recorded in the state of sober calm and supine (digital volume pulse, DVP). The low frequency power in normalized unit (LF), the standardized high frequency power (high frequency power in normalized) and low frequency high frequency power ratio are obtained to evaluate the state of the autonomic nervous system. The blood flow pulse waveform was analyzed to obtain the arterial hardness index (stiffness index, SI) at the four time points. There was no significant difference in the above blood pressure, heart rate variability index and the change of the hardness index between the control night and the experimental night (i.e., whether there was a difference between T2-T1 and C2-C1). If there was a further analysis of these indexes, The changes of CRP, IL-6, TNF-, VEGF, NO, ET-1 in serum were measured before and after night and before and after the experiment night. There was no significant difference between two days and.Spearman correlation analysis was used to analyze the correlation between these indexes.
Results: the actual awakening index of the experimental night was 44 + 9 (27-55.2) per hour. In all sleep structure indexes, the difference of the two nights was statistically significant shorter than that of the control night (P=0.039), and the experimental night ArI was significantly higher than that of the control night (P0.001). The subjects were "awake after waking up". The experimental night was less than the control night (P=0.019), and the awakening times of the experimental night subjects were significantly more than that of the control night (P0.001). The diastolic pressure was significantly higher than that before sleep (P=0.003), and the degree of increase was statistically significant compared with that of the control night (P=0.026); the difference between the diastolic pressure change of the two night and the proportion of the two night N2 sleep The difference had a linear correlation (P=0.011). LF and LHR were significantly higher than before sleep (P0.001), HF was significantly lower than before sleep (P0.001), and the degree of these changes was statistically significant compared with that of the control night (P0.001); the change of HF in experimental night had a linear correlation with the time and proportion of REM sleep (P=0.003, P=0.006); experimental night LHR. There is also a linear correlation with REM sleep time and proportion (P=0.008, P=0.027), and there is no significant difference in the change of.SI at two nights,.CRP, IL-6, TNF- a, VEGF, NO, ET-1 and other serological indexes, there is no significant difference between the two measurements.
Conclusion: repeated awakening by using audio signal stimulation to simulate repeated awakening in OSAHS can cause the increase of sympathetic activity and the decrease of parasympathetic activity, and this change still exists in a period of time after the awakening, suggesting that the effect is accumulative. Repeated awakening leads to the increase of diastolic pressure in the morning, which may be associated with sleep. Structural changes are related, but the significance is not yet clear. In the process of OSAHS related cardiovascular disease, the changes in the state of the autonomic nervous system may be the pathophysiological process earlier than the vascular endothelial dysfunction.
【学位授予单位】：北京协和医学院
【学位级别】：博士
【学位授予年份】：2013
【分类号】：R766
本文编号：2123426
[Abstract]:Objective: This study aims to explore the effect of repeated awakening on the cardiovascular system of healthy subjects, and to identify the status of this pathophysiological process in the process of cardiovascular complications in patients with obstructive sleep apnea syndrome.
Methods: 20 young male healthy subjects (age 25 + 2.1 years old, BMI22.9 + 1.9kg m2) were monitored in the sleep laboratory for two night polysomnography. The first night was the basis control night, and no intervention was done on the subjects. Second night was used to stimulate the experimental night, and the subjects were repeatedly stimulated with audio signals to induce awakening, An audio signal stimulates the whole sleep process. The desired awakening index (arousal index, ArI) is expected to be 60 times per hour. The sleep structure of two nights, subjective sleep quality, blood pressure, heart rate variability, arterial hardness index, and specific serological indexes. Sleep structure indexes including total sleep time, N1, N2, N3, REM, and REM periods are also compared. The ratio and the Arl.St Mary's Hospital Sleep Questionnaire were used to evaluate the quality and continuity of sleep. In the control night before night (C1), after waking up (C2), at night before sleep (T1), after waking up (T2), the blood pressure was measured and the blood flow pulse (Digital volume pulse, DVP) was recorded in the state of sober calm and supine (digital volume pulse, DVP). The low frequency power in normalized unit (LF), the standardized high frequency power (high frequency power in normalized) and low frequency high frequency power ratio are obtained to evaluate the state of the autonomic nervous system. The blood flow pulse waveform was analyzed to obtain the arterial hardness index (stiffness index, SI) at the four time points. There was no significant difference in the above blood pressure, heart rate variability index and the change of the hardness index between the control night and the experimental night (i.e., whether there was a difference between T2-T1 and C2-C1). If there was a further analysis of these indexes, The changes of CRP, IL-6, TNF-, VEGF, NO, ET-1 in serum were measured before and after night and before and after the experiment night. There was no significant difference between two days and.Spearman correlation analysis was used to analyze the correlation between these indexes.
Results: the actual awakening index of the experimental night was 44 + 9 (27-55.2) per hour. In all sleep structure indexes, the difference of the two nights was statistically significant shorter than that of the control night (P=0.039), and the experimental night ArI was significantly higher than that of the control night (P0.001). The subjects were "awake after waking up". The experimental night was less than the control night (P=0.019), and the awakening times of the experimental night subjects were significantly more than that of the control night (P0.001). The diastolic pressure was significantly higher than that before sleep (P=0.003), and the degree of increase was statistically significant compared with that of the control night (P=0.026); the difference between the diastolic pressure change of the two night and the proportion of the two night N2 sleep The difference had a linear correlation (P=0.011). LF and LHR were significantly higher than before sleep (P0.001), HF was significantly lower than before sleep (P0.001), and the degree of these changes was statistically significant compared with that of the control night (P0.001); the change of HF in experimental night had a linear correlation with the time and proportion of REM sleep (P=0.003, P=0.006); experimental night LHR. There is also a linear correlation with REM sleep time and proportion (P=0.008, P=0.027), and there is no significant difference in the change of.SI at two nights,.CRP, IL-6, TNF- a, VEGF, NO, ET-1 and other serological indexes, there is no significant difference between the two measurements.
Conclusion: repeated awakening by using audio signal stimulation to simulate repeated awakening in OSAHS can cause the increase of sympathetic activity and the decrease of parasympathetic activity, and this change still exists in a period of time after the awakening, suggesting that the effect is accumulative. Repeated awakening leads to the increase of diastolic pressure in the morning, which may be associated with sleep. Structural changes are related, but the significance is not yet clear. In the process of OSAHS related cardiovascular disease, the changes in the state of the autonomic nervous system may be the pathophysiological process earlier than the vascular endothelial dysfunction.
【学位授予单位】：北京协和医学院
【学位级别】：博士
【学位授予年份】：2013
【分类号】：R766
【参考文献】
相关期刊论文 前2条
1 钟旭,肖毅,黄蓉,黄席珍;整夜完全睡眠剥夺对心血管自主神经活动的影响[J];中华内科杂志;2005年08期
2 Xu Zhong;Yi Xiao;Rong Huang;;Effects of Obstructive Sleep Apneas on Endothelial Function and Autonomic Modulation in Adult Man[J];Chinese Medical Sciences Journal;2012年04期
，本文编号：2123426
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