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Evaluation of Inflammatory Markers in a Large Sample of Obstructive Sleep Apnea Patients without Comorbidities.评估无合并症的阻塞性睡眠呼吸暂停患者大样本中的炎症标志物。
Mediators Inflamm. 2017;2017:4573756. doi: 10.1155/2017/4573756. Epub 2017 Jul 31.
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Oxidative Stress and Cardiovascular Risk: Obesity, Diabetes, Smoking, and Pollution: Part 3 of a 3-Part Series.氧化应激与心血管风险:肥胖、糖尿病、吸烟及污染:系列文章之三(共三篇)
J Am Coll Cardiol. 2017 Jul 11;70(2):230-251. doi: 10.1016/j.jacc.2017.05.043.
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Impact of Oxidative Stress on the Heart and Vasculature: Part 2 of a 3-Part Series.氧化应激对心脏和血管系统的影响:三部曲系列的第2部分。
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Predictive value of telomere length on outcome following acute myocardial infarction: evidence for contrasting effects of vascular vs. blood oxidative stress.端粒长度对急性心肌梗死后结局的预测价值:血管与血液氧化应激的对比作用证据。
Eur Heart J. 2017 Nov 1;38(41):3094-3104. doi: 10.1093/eurheartj/ehx177.
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Ischemia/Reperfusion Injury following Acute Myocardial Infarction: A Critical Issue for Clinicians and Forensic Pathologists.急性心肌梗死后的缺血/再灌注损伤:临床医生和法医病理学家面临的关键问题。
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The Role of Acute Intermittent Hypoxia in Neutrophil-Generated Superoxide, Sympathovagal Balance, and Vascular Function in Healthy Subjects.急性间歇性低氧对健康受试者中性粒细胞产生超氧化物、交感迷走神经平衡及血管功能的作用
Front Physiol. 2017 Jan 23;8:4. doi: 10.3389/fphys.2017.00004. eCollection 2017.
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Overnight urinary isoprostanes as a marker of oxidative stress in obstructive sleep apnoea.夜间尿中异前列腺素作为阻塞性睡眠呼吸暂停氧化应激的标志物。
Eur Respir J. 2017 Feb 2;49(2). doi: 10.1183/13993003.01787-2016. Print 2017 Feb.
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Effect on Intermittent Hypoxia on Plasma Exosomal Micro RNA Signature and Endothelial Function in Healthy Adults.间歇性低氧对健康成年人血浆外泌体微小RNA特征及内皮功能的影响
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CPAP for Prevention of Cardiovascular Events in Obstructive Sleep Apnea.持续气道正压通气治疗阻塞性睡眠呼吸暂停对心血管事件的预防作用。
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Effect of CPAP Withdrawal on BP in OSA: Data from Three Randomized Controlled Trials.持续气道正压通气撤离对阻塞性睡眠呼吸暂停患者血压的影响:来自三项随机对照试验的数据。
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间歇性缺氧、心血管疾病与阻塞性睡眠呼吸暂停

Intermittent hypoxia, cardiovascular disease and obstructive sleep apnoea.

作者信息

Turnbull Chris D

机构信息

NIHR Oxford Biomedical Research Centre, University of Oxford, Oxford, UK.

Oxford Centre for Respiratory Medicine, Oxford University Hospitals NHS Foundation Trust, Oxford, UK.

出版信息

J Thorac Dis. 2018 Jan;10(Suppl 1):S33-S39. doi: 10.21037/jtd.2017.10.33.

DOI:10.21037/jtd.2017.10.33
PMID:29445526
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5803045/
Abstract

Obstructive sleep apnoea (OSA) is a common disorder and is associated with cardiovascular disease. Continuous positive airway pressure (CPAP), whilst reducing blood pressure, has not been shown to reduce cardiovascular events when used as a treatment solely for this purpose in patients with previous cardiovascular disease. Developing a better understanding of the mechanisms underlying cardiovascular disease in OSA is important to develop new treatments. Potential causative mechanisms for cardiovascular disease in OSA include arousal induced sympathetic activation, large intrathoracic pressure swings leading to shear stress on the heart and great vessels, and intermittent hypoxia (IH). This review discusses the role of IH, as a major physiological consequence of OSA, in the development of cardiovascular disease.

摘要

阻塞性睡眠呼吸暂停(OSA)是一种常见疾病,与心血管疾病相关。持续气道正压通气(CPAP)虽然能降低血压,但在仅用于治疗既往有心血管疾病的患者时,尚未显示能减少心血管事件。更好地了解OSA中心血管疾病的潜在机制对于开发新的治疗方法很重要。OSA中心血管疾病的潜在致病机制包括觉醒诱导的交感神经激活、导致心脏和大血管剪切应力的巨大胸内压力波动以及间歇性缺氧(IH)。本综述讨论了作为OSA主要生理后果的IH在心血管疾病发生发展中的作用。