阻塞性睡眠呼吸暂停合并肺动脉高压肺血管重塑的机制

Mechanism of pulmonary vascular remodeling in obstructive sleep apnea complicated with pulmonary hypertension

阻塞性睡眠呼吸暂停(OSA)是一种多数由上呼吸道,特别是鼻、咽部位的解剖学狭窄导致的,在睡眠状态下反复出现呼吸暂停和/或低通气、睡眠中断,从而使机体发生一系列病理生理改变的临床综合征。OSA是一种常见疾病和多发病,对人类的健康危害极大,尤其是OSA合并肺动脉高压患者预后差。OSA与肺动脉高压密切相关,OSA既可以是肺动脉高压的病因也可以是合并症,因此其发病机制复杂。研究证实,肺动脉重塑在OSA的肺动脉高压的发生、发展过程中起着重要的作用。本综述旨在对近年来肺动脉重塑在OSA合并肺动脉高压形成过程中主要机制的进展进行总结,为临床进一步研究提供参考。

Obstructive sleep apnea(OSA)is mostly caused by anatomical stenosis of the upper respiratory tract,especially the nose and pharynx.Recurrent apnea and(or)hypopnea and sleep interruption occur during sleep.So that the body displays a series of clinical syndromes with pathophysiological changes.OSA is a common and frequently-occurring disease,which is extremely harmful to human health,especially for patients with OSA combined with pulmonary hypertension.The prognosis is poor.OSA is closely related to pulmonary hypertension.OSA can be either the cause or comorbidity of pulmonary hypertension,so its pathogenesis is complicated.Studies have confirmed that pulmonary artery remodeling plays an important role in the occurrence and development of OSA pulmonary hypertension.This review aims to summarize the progress of the main mechanisms of pulmonary artery remodeling in the process of OSA combined with pulmonary hypertension in recent years,and provide a reference for further clinical research.