Guilleminault C, Stoohs R, Shiomi T, Kushida C, Schnittger I
Stanford University Sleep Disorders Center, Palo Alto, Calif., USA.
Chest. 1996 Apr;109(4):901-8. doi: 10.1378/chest.109.4.901.
Upper airway resistance syndrome (UARS) is a sleep-disordered breathing syndrome characterized by complaints of daytime fatigue and/or sleepiness, increased upper airway resistance during sleep, frequent transient arousals, and no significant hypoxemia. Of a population of 110 subjects (58 men) diagnosed as having UARS, we investigated acute systolic and diastolic BP changes seen during sleep in two different samples. First, six patients from the original subject pool were found to have untreated chronic borderline high BP, and were subjected to 48 h of continuous ambulatory BP monitoring before treatment and another 48 h of BP monitoring 1 month after the start of nasal-continuous positive airway pressure (N-CPAP) treatment. Five of six subjects used their equipment on a regular basis and had their chronic borderline high BP completely controlled. No change in BP values was seen in the last subject, who discontinued N-CPAP after 3 days. A second protocol investigated seven normotensive subjects drawn from the initial subject pool. Continuous radial artery BP recording was performed during nocturnal sleep with simultaneous polygraphic recording of sleep/wake variables and respiration. BP changes were studied during periods of increased respiratory efforts and at the time of alpha EEG arousals. Increases in systolic and diastolic BP were noted during the breaths with the greatest inspiratory efforts without significant hypoxemia. A further increase in BP was noted in association with arousals. Three of these subjects also underwent echocardiography during sleep, which demonstrated a leftward shift of the interventricular septum with pulsus paradoxus in association with peak end-inspiratory esophageal pressure more negative than -35 cm H2O. Our study indicates that, in the absence of classic apneas, hypopneas, and repetitive significant drops in oxygen saturation (below 90%), repetitive increases in BP can occur as a result of increased airway resistance during sleep. It also shows that, in some patients with both UARS and borderline high BP, high BP can be controlled with treatment of UARS. We conclude that abnormal upper airway resistance during sleep, often associated with snoring, can play a role in the development of hypertension.
上气道阻力综合征（UARS）是一种睡眠呼吸障碍综合征，其特征为白天疲劳和/或嗜睡、睡眠中上气道阻力增加、频繁短暂觉醒，且无明显低氧血症。在110名被诊断为患有UARS的受试者（58名男性）群体中，我们在两个不同样本中研究了睡眠期间急性收缩压和舒张压的变化。首先，在最初的受试者群体中发现6名患者患有未经治疗的慢性临界高血压，在治疗前对其进行48小时的动态血压监测，并在开始鼻持续气道正压通气（N-CPAP）治疗1个月后再次进行48小时的血压监测。6名受试者中有5名定期使用设备，其慢性临界高血压得到了完全控制。最后一名受试者在3天后停止使用N-CPAP，其血压值未发生变化。第二个方案研究了从最初受试者群体中抽取的7名血压正常的受试者。在夜间睡眠期间进行连续桡动脉血压记录，同时多导记录睡眠/觉醒变量和呼吸情况。在呼吸努力增加期间以及α脑电图觉醒时研究血压变化。在吸气努力最大的呼吸过程中，收缩压和舒张压升高，且无明显低氧血症。与觉醒相关的血压进一步升高。其中3名受试者在睡眠期间还接受了超声心动图检查，结果显示室间隔向左移位，伴有吸气末峰值食管压力比-35 cm H2O更负时的奇脉。我们的研究表明，在没有典型呼吸暂停、呼吸浅慢以及氧饱和度反复显著下降（低于90%）的情况下，睡眠期间气道阻力增加可导致血压反复升高。研究还表明，在一些同时患有UARS和临界高血压的患者中，UARS治疗可控制高血压。我们得出结论，睡眠期间异常的上气道阻力（通常与打鼾有关）可能在高血压的发生发展中起作用。
