Ramar Kannan, Caples Sean M
Mayo Clinic, Center for Sleep Medicine, Division of Pulmonary, Sleep & Critical Care Medicine, Mayo Clinic, Rochester, MN, USA.
Future Cardiol. 2011 Mar;7(2):241-9. doi: 10.2217/fca.10.123.
Vascular changes related to obstructive sleep apnea (OSA) can lead to chronic cardiovascular consequences such as hypertension. The cardiovascular consequences are owing to nocturnal perturbations related to intrathoracic pressure changes, intermittent hypoxia, sympathetic neural activation, endothelial dysfunction, oxidative stress and systemic inflammation. Intermittent hypoxia due to sleep-related events in OSA activates the renin-angiotensin system and increases the levels of endothelin-1. Intermittent hypoxia also results in oxidative stress, as evidenced by elevated levels of xanthine oxidoreductase, lipid peroxidation and the presence of reactive oxygen species. There is also evidence for a decrease in antioxidant capacity. Patients with OSA may have endothelial dysfunction that resolves with continuous positive airway pressure. OSA is a state of inflammation as evidenced by elevated levels of C-reactive protein, IL-6, NF-κB, TNF-α, ICAM-1, VCAM-1 and E-selectin. This may suggest that OSA is a predisposing factor for atherogenesis. This article will discuss the role of nocturnal perturbations consequent to OSA resulting in endothelial dysfunction, oxidative stress, and inflammation and how they may subsequently play a causative role in cardiovascular disorders.
与阻塞性睡眠呼吸暂停（OSA）相关的血管变化可导致慢性心血管后果，如高血压。这些心血管后果归因于与胸内压变化、间歇性缺氧、交感神经激活、内皮功能障碍、氧化应激和全身炎症相关的夜间干扰。OSA中与睡眠相关事件导致的间歇性缺氧会激活肾素-血管紧张素系统并增加内皮素-1的水平。间歇性缺氧还会导致氧化应激，黄嘌呤氧化还原酶水平升高、脂质过氧化和活性氧的存在证明了这一点。也有证据表明抗氧化能力下降。OSA患者可能存在内皮功能障碍，持续气道正压通气可使其得到缓解。OSA是一种炎症状态，C反应蛋白、IL-6、NF-κB、TNF-α、ICAM-1、VCAM-1和E-选择素水平升高证明了这一点。这可能表明OSA是动脉粥样硬化的一个易感因素。本文将讨论OSA导致的夜间干扰在引起内皮功能障碍、氧化应激和炎症方面的作用，以及它们随后如何在心血管疾病中发挥致病作用。
