Narkiewicz K, Somers V K
Department of Hypertension and Diabetology, Medical University of Gdańsk, Debinki, Poland.
Acta Physiol Scand. 2003 Mar;177(3):385-90. doi: 10.1046/j.1365-201X.2003.01091.x.
The mechanisms underlying the link between obstructive sleep apnoea (OSA) and cardiovascular disease are not completely established. However, there is increasing evidence that autonomic mechanisms are implicated. A number of studies have consistently shown that patients with OSA have high levels of sympathetic nerve traffic. During sleep, repetitive episodes of hypoxia, hypercapnia and obstructive apnoea act through chemoreceptor reflexes and other mechanisms to increase sympathetic drive. Remarkably, the high sympathetic drive is present even during daytime wakefulness when subjects are breathing normally and no evidence of hypoxia or chemoreflex activation is apparent. Several neural and humoral mechanisms may contribute to maintenance of higher sympathetic activity and blood pressure. These mechanisms include chemoreflex and baroreflex dysfunction, altered cardiovascular variability, vasoconstrictor effects of nocturnal endothelin release and endothelial dysfunction. Long-term continuous positive airway pressure treatment decreases muscle sympathetic nerve activity in OSA patients. The vast majority of OSA patients remain undiagnosed. Unrecognized OSA may contribute, in part, to the metabolic and cardiovascular derangements that are thought to be linked to obesity, and to the association between obesity and cardiovascular risk. Furthermore, acting through sympathetic neural mechanisms, OSA may contribute to or augment elevated levels of blood pressure in a large proportion of the hypertensive patient population.
阻塞性睡眠呼吸暂停（OSA）与心血管疾病之间联系的潜在机制尚未完全明确。然而，越来越多的证据表明自主神经机制与之相关。多项研究一致表明，OSA患者的交感神经活动水平较高。在睡眠期间，反复出现的低氧血症、高碳酸血症和阻塞性呼吸暂停通过化学感受器反射及其他机制增加交感神经驱动力。值得注意的是，即使在白天清醒时，当受试者呼吸正常且无低氧血症或化学反射激活迹象时，高交感神经驱动力依然存在。多种神经和体液机制可能导致较高的交感神经活动和血压维持在较高水平。这些机制包括化学反射和压力反射功能障碍、心血管变异性改变、夜间内皮素释放的血管收缩作用以及内皮功能障碍。长期持续气道正压通气治疗可降低OSA患者的肌肉交感神经活动。绝大多数OSA患者仍未被诊断出来。未被识别的OSA可能部分导致了被认为与肥胖相关的代谢和心血管紊乱，以及肥胖与心血管风险之间的关联。此外，通过交感神经机制，OSA可能在很大一部分高血压患者人群中导致或加剧血压升高。
