氧气、二氧化碳和一氧化氮：在阻塞性睡眠呼吸暂停病理生理学中的作用。

文献信息

中文摘要

阻塞性睡眠呼吸暂停是一种常见的睡眠相关呼吸障碍，睡眠期间反复发生上气道塌陷，导致周期性血气波动。氧气、二氧化碳和一氧化氮在其病理生理学中起关键作用。本叙述性综述旨在探讨气体在阻塞性睡眠呼吸暂停病理生理学中的作用，重点关注慢性间歇性低氧、间歇性高碳酸血症和一氧化氮失调的分子通路及效应。慢性间歇性低氧刺激缺氧诱导因子-1α等分子通路和核因子κB等炎症级联反应，导致氧化应激、内皮功能障碍和交感神经过度激活。间歇性高碳酸血症影响化学反射敏感性、通气不稳定性和自主神经功能，新出现的证据表明其既有致病作用也可能有益。一氧化氮调节气道张力、血管反应性和免疫控制，在阻塞性睡眠呼吸暂停患者中其生物利用度降低。这三种气体介质促成了阻塞性睡眠呼吸暂停复杂的病理生理学，并构成了该病长期心血管、代谢和神经认知风险的基础。适当优先考虑这些气体与阻塞性睡眠呼吸暂停病理生理学之间的关系，有助于对该病的新认识和未来的新治疗方法。

英文摘要

Obstructive sleep apnea is a prevalent sleep-related breathing disorder with recurrent episodes of upper airway collapse during sleep, leading to cyclic blood gas fluctuations. Oxygen, carbon dioxide, and nitric oxide play a crucial role in the pathophysiology. This narrative review aims to explore the role of gases in obstructive sleep apnea pathophysiology, focusing on the molecular pathways and effects of chronic intermittent hypoxia, intermittent hypercapnia, and nitric oxide dysregulation. Chronic intermittent hypoxia stimulates molecular pathways such as hypoxia-inducible factor-1α and inflammatory cascades such as nuclear factor kappa B, leading to oxidative stress, endothelial dysfunction, and sympathetic overactivation. Intermittent hypercapnia impacts on chemoreflex sensitivity, ventilatory instability, and autonomic function, with emerging evidence of both pathogenic and potentially beneficial effects. Nitric oxide, which modulates airway tone, vascular reactivity, and immune control, presents a reduced bioavailability in patients with obstructive sleep apnea. These three gas mediators contribute to the complex pathophysiology of obstructive sleep apnea and underlie the long-term cardiovascular, metabolic, and neurocognitive risks of obstructive sleep apnea. Appropriately prioritizing the relationship between these gases and the pathophysiology of obstructive sleep apnea contributes to a new understanding of the disease and new treatment approaches in the future.