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阻塞性睡眠呼吸暂停:间歇性低氧和炎症的作用。

Obstructive sleep apnea: role of intermittent hypoxia and inflammation.

机构信息

Division of Pulmonary, Critical Care and Sleep Medicine, University Hospitals Case Medical Center, Cleveland, Ohio.

Neurologic Institute, Respiratory Institute, Heart and Vascular Institute and Lerner Research Institute, Cleveland Clinic Lerner College of Medicine of Case Western Research University, Cleveland Clinic Foundation, Cleveland, Ohio.

出版信息

Semin Respir Crit Care Med. 2014 Oct;35(5):531-44. doi: 10.1055/s-0034-1390023. Epub 2014 Oct 21.

DOI:10.1055/s-0034-1390023
PMID:25333334
Abstract

Obstructive sleep apnea results in intermittent hypoxia via repetitive upper airway obstruction leading to partial or complete upper airway closure, apneas and hypopneas, respectively. Intermittent hypoxia leads to sympathetic nervous system activation and oxidative stress with a resultant systemic inflammatory cascade. The putative mechanism by which obstructive sleep apnea has been linked to numerous pathologic conditions including stoke, cardiovascular disease, hypertension, and metabolic derangements is through these systemic effects. Treatment of obstructive sleep apnea appears to reduce systemic markers of inflammation and ameliorates the adverse sequelae of this disease.

摘要

阻塞性睡眠呼吸暂停通过反复的上呼吸道阻塞导致部分或完全上呼吸道关闭,分别导致呼吸暂停和低通气。间歇性低氧导致交感神经系统激活和氧化应激,从而导致全身炎症级联反应。阻塞性睡眠呼吸暂停与多种病理状况(包括中风、心血管疾病、高血压和代谢紊乱)相关的潜在机制是通过这些全身效应。阻塞性睡眠呼吸暂停的治疗似乎可以降低全身炎症标志物,并改善这种疾病的不良后果。

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