Division of Pulmonary, Critical Care, & Sleep Medicine, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, United States.
Respir Physiol Neurobiol. 2012 Nov 15;184(2):192-6. doi: 10.1016/j.resp.2012.08.011. Epub 2012 Aug 21.
Obstructive sleep apnea is a common disease, affecting 16% of the working age population. Although sleep apnea has a well-established connection to daytime sleepiness presumably mediated through repetitive sleep disruption, some other consequences are less well understood. Clinical, epidemiological, and physiological investigations have demonstrated a connection between sleep apnea and daytime hypertension. The elevation of arterial pressure is evident during waking, when patients are not hypoxic, and is mediated by sustained sympathoexcitation and by altered peripheral vascular reactivity. This review summarizes data suggesting that both the sympathoexcitation and the altered vascular reactivity are, at least in part, a consequence of reduced expression of nitric oxide synthase, in neural tissue and in endothelium. Reduced nitric oxide generation in central and peripheral sites of sympathoregulation and in endothelium together may, in part, explain the elevations in waking pressures observed in sleep apnea patients.
阻塞性睡眠呼吸暂停是一种常见疾病，影响了 16%的工作年龄人群。尽管睡眠呼吸暂停与日间嗜睡有明确的关联，这种关联可能是通过反复的睡眠中断介导的，但其他一些后果还不太清楚。临床、流行病学和生理学研究已经证实了睡眠呼吸暂停与日间高血压之间的联系。当患者不缺氧时，动脉压在清醒期间升高，这是由持续的交感兴奋和外周血管反应性改变介导的。这篇综述总结了一些数据，表明交感兴奋和血管反应性的改变至少部分是由于一氧化氮合酶在神经组织和内皮中的表达减少所致。中枢和外周交感调节部位以及内皮细胞中一氧化氮生成减少，可能部分解释了睡眠呼吸暂停患者清醒时血压升高的原因。
