Atkeson Amy, Jelic Sanja
Division of Pulmonary, Allergy, and Critical Care Medicine, Columbia University College of Physicians and Surgeons, 630 West 168th Street, New York, NY 10032, USA.
Vasc Health Risk Manag. 2008;4(6):1327-35. doi: 10.2147/vhrm.s4078.
Endothelial activation and inflammation are important mediators of accelerated atherogenesis and consequent increased cardiovascular morbidity in obstructive sleep apnea (OSA). Repetitive episodes of hypoxia/reoxygenation associated with transient cessation of breathing during sleep in OSA resemble ischemia/reperfusion injury and may be the main culprit underlying endothelial dysfunction in OSA. Additional factors such as repetitive arousals resulting in sleep fragmentation and deprivation and individual genetic susceptibility to vascular manifestations of OSA contribute to impaired endothelial function in OSA. The present review focuses on possible mechanisms that underlie endothelial activation and inflammation in OSA.
内皮细胞激活与炎症是阻塞性睡眠呼吸暂停（OSA）中动脉粥样硬化加速及心血管疾病发病率随之增加的重要介导因素。与OSA睡眠期间呼吸短暂停止相关的反复缺氧/复氧发作类似于缺血/再灌注损伤，可能是OSA内皮功能障碍的主要原因。其他因素，如导致睡眠片段化和剥夺的反复觉醒以及个体对OSA血管表现的遗传易感性，也会导致OSA内皮功能受损。本综述重点关注OSA中内皮细胞激活与炎症的潜在机制。
