Does episodic hypoxia affect upper airway dilator muscle function? Implications for the pathophysiology of obstructive sleep apnoea
Does episodic hypoxia affect upper airway dilator muscle function? Implications for the pathophysiology of obstructive sleep apnoea
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DOI：
10.1016/j.resp.2005.04.001
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发表时间：
2005-07-28
影响因子：
2.3
通讯作者：
O'Halloran, KD
中科院分区：
文献类型：
--
作者：
Bradford, A;McGuire, M;O'Halloran, KD
阻塞性睡眠呼吸暂停（OSA）的特征在于睡眠期间由于上气道肌肉活动的睡眠相关的减少而导致上气道的反复塌陷，随后咽扩张肌无法抵抗吸气期间由隔膜和副肌产生的塌陷压力。睡眠期间上呼吸道阻塞的原因是多方面的，但有证据表明，在OSA的病理生理学中，上呼吸道肌肉的内在功能和中枢调节受损。这种情况与复发性呼吸暂停引起的间歇性缺氧有关。然而，尽管其明显的重要性是很少有人知道的影响，间歇性缺氧上气道muscle function.In这篇综述中，我们研究的证据表明，慢性间歇性缺氧可以影响上气道肌肉的结构和功能，并损害中枢神经系统控制的咽扩张肌。我们回顾了文献，并讨论了我们实验室的结果，这些结果表明，间歇性缺氧/窒息会降低上气道肌肉耐力，并选择性地损害咽扩张肌对生理刺激的肌电图反应。我们的观察使我们推测，间歇性缺氧--周期性气道阻塞的结果--通过调节上呼吸道开放的神经控制系统受损和通过改变呼吸肌收缩，功能，导致建立进一步的气道阻塞和缺氧损伤的恶性循环，慢性加重和延续病情。我们的结论是，慢性间歇性缺氧/窒息有助于睡眠呼吸障碍的病理生理。(C)2005 Elsevier B. V.保留所有权利。
Obstructive sleep apnoea (OSA) is characterised by repetitive collapse of the upper airway during sleep owing to a sleep-related decrement in upper airway muscle activity with consequent failure of the pharyngeal dilator muscles to oppose the collapsing pressure that is generated by the diaphragm and accessory muscles during inspiration. The causes of upper airway obstruction during sleep are multi-factorial but there is evidence implicating intrinsic upper airway muscle function and impaired central regulation of the upper airway muscles in the pathophysiology of OSA. The condition is associated with episodic hypoxia due to recurrent apnoea. However, despite its obvious importance very little is known about the effects of episodic hypoxia on upper airway muscle function.In this review, we examine the evidence that chronic intermittent hypoxia can affect upper airway muscle structure and function and impair CNS control of the pharyngeal dilator muscles. We review the literature and discuss results from our laboratory showing that episodic hypoxia/asphyxia reduces upper airway muscle endurance and selectively impairs pharyngeal dilator EMG responses to physiological stimulation.Our observations lead us to speculate that episodic hypoxia - a consequence of periodic airway occlusion - is responsible for progression of OSA through impairment of the neural control systems that regulate upper airway patency and through altered respiratory muscle contractile function, leading to the establishment of a vicious cycle of further airway obstruction and hypoxic insult that chronically exacerbates and perpetuates the condition. We conclude that chronic intermittent hypoxia/asphyxia contributes to the pathophysiology of sleep-disordered breathing. (C) 2005 Elsevier B.V. All rights reserved.