作者：王连辉，元小冬，徐斌，马倩，张萍淑

单位：

1.河北北方学院2.开滦总医院神经内科3.河北省神经生物机能重点实验室

Units：

1.Hebei North University, Zhangjiakou 075000, China 2.Neurological Department, Kailuan General Hospital, Tangshan 063000, China 3.Hebei Key Laboratory of Neurobiological Function, Tangshan 063000, China

关键词：

睡眠呼吸暂停,阻塞性; 阻塞性睡眠呼吸暂停综合征; 卒中; 动脉粥样硬化; 综述;

Keywords：

　Sleep apnea, obstructive; Obstructive sleep apnea-hypopnea syndrome; Stroke; Atherosclerosis; Review

CLC：

DOI：

10.12114/j.issn.1008-5971.2023.00.089

Funds：

2020年度河北省重点研发计划项目（203777116D）

摘要：

阻塞性睡眠呼吸暂停低通气综合征（OSAHS）是常见的睡眠相关呼吸障碍，近年来其发病率较高，因其会影响患者的生活质量而受到越来越多学者的关注。多项研究表明，动脉粥样硬化是OSAHS患者发生缺血性卒中的重要机制。本文综述了OSAHS患者发生动脉粥样硬化的主要机制：长期间歇性缺氧-复氧会激活炎症途径，导致炎性细胞与下游前炎性细胞因子、趋化因子和黏附分子表达增加，加上氧化应激、内皮功能损伤等最终导致动脉粥样硬化的发生发展，进而增加卒中的发生风险。此外，本研究还指出OSAHS合并卒中患者存在睡眠周期紊乱、脑血流自动调节功能改变、认知障碍等表现，这对OSAHS合并卒中患者的管理具有一定参考价值。

Abstract：

Obstructive sleep apnea hypopnea syndrome (OSAHS) is a common sleep-related respiratory disorder. In recent years, its incidence is high, and it has attracted more and more scholars' attention because it affects the quality of life of patients. Many studies have shown that atherosclerosis is an important mechanism of ischemic stroke in OSAHS patients. This article reviews the main mechanisms of atherosclerosis in OSAHS patients: long-term intermittent hypoxia-reoxygenation will activate the inflammatory pathway, induce increased expression of inflammatory cells and downstream pro-inflammatory cytokines, chemokines and adhesion molecules, coupled with oxidative stress, endothelial dysfunction, etc. Eventually lead to the occurrence and development of atherosclerosis, thereby increasing the risk of stroke. In addition, OSAHS patients with stroke also have sleep cycle disorders, changes in cerebral blood flow autoregulation, and cognitive impairment, it has certain reference value for the management of OSAHS patients with stroke.

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