Atkeson Amy, Yeh Susie Yim, Malhotra Atul, Jelic Sanja
Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, New York, NY 10032, USA.
Prog Cardiovasc Dis. 2009 Mar-Apr;51(5):351-62. doi: 10.1016/j.pcad.2008.08.002.
Untreated obstructive sleep apnea (OSA) is an independent risk factor for hypertension, myocardial infarction, and stroke. The repetitive hypoxia/reoxygenation and sleep fragmentation associated with OSA impair endothelial function. Endothelial dysfunction, in turn, may mediate increased risk for cardiovascular diseases. Specifically, in OSA, endothelial nitric oxide availability and repair capacity are reduced, whereas oxidative stress and inflammation are enhanced. Treatment of OSA improves endothelial vasomotor tone and reduces inflammation. We review the evidence and possible mechanisms of endothelial dysfunction as well as the effect of treatment on endothelial function in OSA.
未经治疗的阻塞性睡眠呼吸暂停（OSA）是高血压、心肌梗死和中风的独立危险因素。与OSA相关的反复缺氧/复氧和睡眠片段化会损害内皮功能。内皮功能障碍反过来可能介导心血管疾病风险增加。具体而言，在OSA中，内皮一氧化氮的可用性和修复能力降低，而氧化应激和炎症增强。OSA的治疗可改善内皮血管舒缩张力并减轻炎症。我们综述了OSA中内皮功能障碍的证据和可能机制，以及治疗对内皮功能的影响。
