Endothelial dysfunction in adults with obstructive sleep apnea.
Endothelial dysfunction in adults with obstructive sleep apnea.
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DOI：
10.1159/000325108
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发表时间：
2011-01-01
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血管内皮功能障碍是指血管中正常稳态功能的丧失。其特点是血管舒张功能减少、血管收缩功能增强以及慢性血栓形成和炎症活动。有令人信服的证据表明阻塞性睡眠呼吸暂停 (OSA) 会导致内皮功能障碍：OSA 与血管结构及其弹性特性的改变、循环细胞衍生微粒增加、内皮修复能力降低和血管反应性相关。这些改变可能与一氧化氮的可用性降低有关，一氧化氮具有主要的血管保护作用，包括血管舒张、抑制血小板粘附和聚集、抑制白细胞-内皮粘附和抑制平滑肌细胞增殖。目前尚不清楚 OSA 中的内皮功能障碍是否是由于与血管紧张素 II 或内皮素 1 相关的血管收缩机制的改变所致。在 OSA 中，内皮功能障碍可能与慢性间歇性缺氧以及睡眠不足和睡眠不足有关。这些情况可能会增加各种炎症和氧化应激标志物的水平，以及促凝血和血栓形成活性增加的标志物水平。此外，它们还可能导致血管舒缩功能失衡。内皮功能障碍导致动脉粥样硬化和与 OSA 相关的心血管疾病的发生。然而，其他也与内皮功能障碍相关的疾病是 OSA 合并症，例如：肥胖、胰岛素抵抗、吸烟习惯和心血管疾病，如高血压和冠状动脉疾病。这使得很难证明 OSA 与内皮功能障碍之间的因果关系；然而，治疗研究已经提供了这种联系的证据。持续气道正压通气可能会逆转与内皮功能障碍相关的变化，因此可能会降低 OSA 患者患心血管疾病的风险。
Vascular endothelial dysfunction refers to a loss of normal homeostatic functions in the blood vessels. It is characterized by reduced vasodilation and enhanced vasoconstriction functions and chronic prothrombotic and inflammatory activity. There is convincing evidence for endothelial dysfunction in obstructive sleep apnea (OSA): OSA is associated with alterations in vascular structures and their elastic properties, increased circulating cell-derived microparticles, reduced endothelial repair capacity, and vascular reactivity. These alterations may be related to the reduced availability of nitric oxide, which has major vasoprotective effects including vasodilation, inhibition of platelet adhesion and aggregation, inhibition of leukocyte-endothelial adhesion and inhibition of smooth muscle cell proliferation. It is unknown whether endothelial dysfunction in OSA is due to alterations in vasoconstriction mechanisms related to angiotensin II or endothelin 1. In OSA, endothelial dysfunction may be related to chronic intermittent hypoxia and to sleep loss and fragmentation. These conditions may increase the levels of various markers of inflammation and oxidative stress, as well as those of increased procoagulant and thrombotic activity. In addition, they may produce an imbalance of vasomotor function. Endothelial dysfunction contributes to the development of atherosclerosis and cardiovascular disorders associated with OSA. However, other diseases that are also associated with endothelial dysfunction are OSA comorbidities, e.g. obesity, insulin resistance, smoking habits and cardiovascular diseases such as hypertension and coronary artery disease. This makes it difficult to demonstrate a causal link between OSA and endothelial dysfunction; nevertheless, evidence for such a link has been produced by therapeutic studies. The administration of continuous positive airway pressure may reverse changes associated with endothelial dysfunction and, therefore, may decrease the risk of cardiovascular disease in OSA patients.