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阻塞性睡眠呼吸暂停中的内皮功能障碍

Endothelial dysfunction in obstructive sleep apnea.

作者信息

Budhiraja Rohit, Parthasarathy Sairam, Quan Stuart F

机构信息

Division of Pulmonary and Critical Care, Department of Medicine, Southern Arizona Veterans Affairs Health Care System, Tucson, AZ 85723, USA.

出版信息

J Clin Sleep Med. 2007 Jun 15;3(4):409-15.

Abstract

Obstructive sleep apnea (OSA) is a common disorder and is associated with adverse cardiovascular consequences, including hypertension and coronary artery disease. While the mechanisms responsible for increased risk of cardiovascular events in OSA have not yet been fully elucidated, hypoxia, inflammation, obesity, metabolic dysregulation, and sympathetic activation, may contribute to these consequences. Endothelial dysfunction may be another link between OSA and cardiovascular disease. Dysfunctional endothelium is characterized by an imbalance in production of vasoactive hormones, increased adherence of inflammatory mediators to endothelial cells and hypercoagulability, and is a known risk factor for cardiovascular events. Studies have directly measured vascular endothelial function in patients with OSA and found a muted response compared to controls. Other studies have evaluated biochemical markers of endothelial function including circulating levels of vasoactive and thrombosis mediators and provide further proof of endothelial dysfunction in this disorder. A better appreciation of the role of the dysfunctional endothelium in OSA will help shed light on the pathogenesis of cardiovascular disease in this disorder and may lead to development of novel therapies aimed at preventing untoward outcomes.

摘要

阻塞性睡眠呼吸暂停(OSA)是一种常见疾病,与不良心血管后果相关,包括高血压和冠状动脉疾病。虽然导致OSA患者心血管事件风险增加的机制尚未完全阐明,但缺氧、炎症、肥胖、代谢失调和交感神经激活可能导致这些后果。内皮功能障碍可能是OSA与心血管疾病之间的另一个联系。功能失调的内皮的特征是血管活性激素产生失衡、炎症介质与内皮细胞的粘附增加以及高凝状态,并且是心血管事件的已知危险因素。研究直接测量了OSA患者的血管内皮功能,发现与对照组相比反应减弱。其他研究评估了内皮功能的生化标志物,包括血管活性和血栓形成介质的循环水平,并为这种疾病中的内皮功能障碍提供了进一步的证据。更好地认识功能失调的内皮在OSA中的作用将有助于阐明这种疾病中心血管疾病的发病机制,并可能导致开发旨在预防不良后果的新疗法。

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