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Obstructive sleep apnoea and the autonomic nervous system.
Sleep Medicine Reviews ( IF 11.2 ) Pub Date : 2004-08-18 , DOI: 10.1016/s1087-0792(98)90001-6
R P Smith 1 , D Veale , J L Pépin , P A Lévy
Affiliation  

Understanding of the pathophysiology of obstructive sleep apnoea, a common yet relatively newly recognized condition, has advanced rapidly in recent years. This condition produces major acute haemodynamic changes and causal relationships with hypertension and cardiovascular morbidity have been proposed. The role that the autonomic nervous system plays in mediating these cardiovascular changes has been the focus of intensive research activity and the development of few techniques in physiological monitoring, such as spectral analysis of heart rate variability, Finapres blood pressure monitoring, measurement of muscle sympathetic nerve activity, radionuclide tests and animal models of obstructive sleep apnoea have substantially increased the knowledge base. The acute haemodynamic changes are associated with high levels of sympathetic discharge and with fluctuating parasympathetic activity. There are also chronic changes in baroreceptor and chemoreceptor reflexes associated with an increase in baseline daytime sympathetic activity and abnormal vagal reflex responses to voluntary respiratory manoeuvres. These acute autonomic changes appear to be provoked by a combination of stimuli triggered by hypoxaemia, upper airway responses, ventilatory changes and arousal. The mechanisms of the chronic autonomic changes are less clear; it is likely that recurrent hypoxaemia is important, but the roles of recurrent ventilatory stress and arousal are not clear. Normalizing respiration with CPAP therapy prevents the acute cardiovascular changes and reduces the acute sympathetic over-activity, and in compliant patients, restores abnormal vagal responses to normal and reduces excess chronic sympathetic activity. Whether or not this produces a reduction in long-term cardiovascular morbidity is not established.

中文翻译:

阻塞性睡眠呼吸暂停和自主神经系统。

阻塞性睡眠呼吸暂停的病理生理学理解是一种常见的但相对较新认识的疾病,近年来已迅速发展。这种情况会导致严重的急性血液动力学变化,并且已经提出与高血压和心血管疾病的因果关系。自主神经系统在介导这些心血管变化中的作用一直是深入研究活动的重点,也是生理监测中一些技术的发展的重点,例如心率变异性的频谱分析,Finapres血压监测,肌肉交感神经测量活动,放射性核素测试和阻塞性睡眠呼吸暂停的动物模型已大大增加了知识库。急性血流动力学改变与高水平的交感神经放电和波动的副交感神经活动有关。压力感受器和化学感受器反射也存在慢性变化,与基线白天交感活动增加和对自主呼吸动作的迷走神经反射反应异常有关。这些急性的自主神经改变似乎是由低氧血症,上呼吸道反应,通气改变和唤醒引起的刺激引起的。慢性自主神经改变的机制尚不清楚。复发性低氧血症很可能很重要,但复发性通气压力和唤醒的作用尚不清楚。通过CPAP治疗使呼吸正常化可防止急性心血管变化并减少急性交感神经过度活动,在依从性患者中,可以使迷走神经反应恢复正常,并减少过多的慢性交感神经活动。尚不确定是否会降低长期心血管疾病的发病率。
更新日期:2019-11-01
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