Endothelial dysfunction in adults with obstructive sleep apnea.

Advances in Cardiology Pub Date : 2011-01-01 Epub Date: 2011-10-13 DOI:10.1159/000325108
{"title":"Endothelial dysfunction in adults with obstructive sleep apnea.","authors":"","doi":"10.1159/000325108","DOIUrl":null,"url":null,"abstract":"<p><p>Vascular endothelial dysfunction refers to a loss of normal homeostatic functions in the blood vessels. It is characterized by reduced vasodilation and enhanced vasoconstriction functions and chronic prothrombotic and inflammatory activity. There is convincing evidence for endothelial dysfunction in obstructive sleep apnea (OSA): OSA is associated with alterations in vascular structures and their elastic properties, increased circulating cell-derived microparticles, reduced endothelial repair capacity, and vascular reactivity. These alterations may be related to the reduced availability of nitric oxide, which has major vasoprotective effects including vasodilation, inhibition of platelet adhesion and aggregation, inhibition of leukocyte-endothelial adhesion and inhibition of smooth muscle cell proliferation. It is unknown whether endothelial dysfunction in OSA is due to alterations in vasoconstriction mechanisms related to angiotensin II or endothelin 1. In OSA, endothelial dysfunction may be related to chronic intermittent hypoxia and to sleep loss and fragmentation. These conditions may increase the levels of various markers of inflammation and oxidative stress, as well as those of increased procoagulant and thrombotic activity. In addition, they may produce an imbalance of vasomotor function. Endothelial dysfunction contributes to the development of atherosclerosis and cardiovascular disorders associated with OSA. However, other diseases that are also associated with endothelial dysfunction are OSA comorbidities, e.g. obesity, insulin resistance, smoking habits and cardiovascular diseases such as hypertension and coronary artery disease. This makes it difficult to demonstrate a causal link between OSA and endothelial dysfunction; nevertheless, evidence for such a link has been produced by therapeutic studies. The administration of continuous positive airway pressure may reverse changes associated with endothelial dysfunction and, therefore, may decrease the risk of cardiovascular disease in OSA patients.</p>","PeriodicalId":50954,"journal":{"name":"Advances in Cardiology","volume":"46 ","pages":"139-170"},"PeriodicalIF":0.0000,"publicationDate":"2011-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000325108","citationCount":"67","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in Cardiology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1159/000325108","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2011/10/13 0:00:00","PubModel":"Epub","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 67

Abstract

Vascular endothelial dysfunction refers to a loss of normal homeostatic functions in the blood vessels. It is characterized by reduced vasodilation and enhanced vasoconstriction functions and chronic prothrombotic and inflammatory activity. There is convincing evidence for endothelial dysfunction in obstructive sleep apnea (OSA): OSA is associated with alterations in vascular structures and their elastic properties, increased circulating cell-derived microparticles, reduced endothelial repair capacity, and vascular reactivity. These alterations may be related to the reduced availability of nitric oxide, which has major vasoprotective effects including vasodilation, inhibition of platelet adhesion and aggregation, inhibition of leukocyte-endothelial adhesion and inhibition of smooth muscle cell proliferation. It is unknown whether endothelial dysfunction in OSA is due to alterations in vasoconstriction mechanisms related to angiotensin II or endothelin 1. In OSA, endothelial dysfunction may be related to chronic intermittent hypoxia and to sleep loss and fragmentation. These conditions may increase the levels of various markers of inflammation and oxidative stress, as well as those of increased procoagulant and thrombotic activity. In addition, they may produce an imbalance of vasomotor function. Endothelial dysfunction contributes to the development of atherosclerosis and cardiovascular disorders associated with OSA. However, other diseases that are also associated with endothelial dysfunction are OSA comorbidities, e.g. obesity, insulin resistance, smoking habits and cardiovascular diseases such as hypertension and coronary artery disease. This makes it difficult to demonstrate a causal link between OSA and endothelial dysfunction; nevertheless, evidence for such a link has been produced by therapeutic studies. The administration of continuous positive airway pressure may reverse changes associated with endothelial dysfunction and, therefore, may decrease the risk of cardiovascular disease in OSA patients.

成人阻塞性睡眠呼吸暂停患者的内皮功能障碍。
血管内皮功能障碍是指血管中正常稳态功能的丧失。它的特点是血管舒张功能降低,血管收缩功能增强,慢性血栓前形成和炎症活动。阻塞性睡眠呼吸暂停(OSA)的内皮功能障碍有令人信服的证据:OSA与血管结构及其弹性特性的改变、循环细胞源性微粒的增加、内皮修复能力的降低和血管反应性有关。这些改变可能与一氧化氮的可用性降低有关,一氧化氮具有主要的血管保护作用,包括血管舒张、抑制血小板粘附和聚集、抑制白细胞内皮粘附和抑制平滑肌细胞增殖。目前尚不清楚OSA患者的内皮功能障碍是否与血管紧张素II或内皮素1相关的血管收缩机制改变有关。在阻塞性睡眠呼吸暂停中,内皮功能障碍可能与慢性间歇性缺氧、睡眠缺失和碎片化有关。这些情况可能会增加各种炎症和氧化应激标志物的水平,以及那些增加的促凝剂和血栓活性。此外,它们还可能造成血管舒缩功能的不平衡。内皮功能障碍有助于与OSA相关的动脉粥样硬化和心血管疾病的发展。然而,与内皮功能障碍相关的其他疾病是OSA合并症,如肥胖、胰岛素抵抗、吸烟习惯和心血管疾病,如高血压和冠状动脉疾病。这使得很难证明OSA和内皮功能障碍之间的因果关系;然而,治疗研究已经提供了这种联系的证据。持续气道正压可逆转与内皮功能障碍相关的变化,因此可降低OSA患者心血管疾病的风险。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
自引率
0.00%
发文量
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信