Update in sleep and control of ventilation 2006

Update in sleep and control of ventilation 2006
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DOI:
10.1164/rccm.200701-043up
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发表时间:
2007-03-01
影响因子:
24.7
通讯作者:
Bradley, T. Douglas
Bradley, T. Douglas
中科院分区:
医学1区
文献类型:
--
作者:
Horner, Richard L.;Bradley, T. Douglas

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虽然阻塞性睡眠呼吸暂停(OSA)患儿的上气道比对照组更易折叠,但大多数OSA患儿在夜间呼吸稳定的时间较长。解剖因素和对负荷产生强大的神经肌肉代偿反应的能力对OSA的发病机制都很重要,后者尤其与恢复充足气流和维持稳定呼吸的能力有关。因此,Katz及其同事(1)通过记录正常、健康、睡眠儿童的颏舌肌活动,确定了神经肌肉代偿性咽扩张肌对气道塌陷压力的反应。受试者(年龄范围9.1-16.4岁,平均11.9岁,体重指数在第70百分位)被置于3 cm H2O的持续气道正压通气(CPAP)上,然后在睡眠期间将面罩压力变化到至少22 cm H2O,连续呼吸5次,并在干预之间恢复到基线30秒。在睡眠中,颏舌肌对气道塌陷压力的反应程度存在广泛的主体间变异性。重要的是,在一些受试者中,颏舌肌活动的显著增加与负荷时气流增加、呼吸频率增加和气流阻力降低有关,在某些情况下,正常通气的恢复没有皮层电唤醒的证据。作者推测,这种强劲的咽扩张肌对负荷的反应可能解释了一些OSA儿童睡眠时稳定呼吸的时间,并且特定儿童睡眠呼吸暂停的严重程度受到内在解剖因素(气道大小和僵硬)、神经肌肉对负荷的补偿反应和唤醒阈值之间的平衡的影响。在清醒状态下,而不是在睡眠状态下,有一种强直动力激活呼吸肌,这一概念在呼吸医学中一直是一个重要而持久的概念,尤其是因为它是理解睡眠对呼吸的影响和睡眠相关呼吸障碍(如OSA)发病机制的根本机制。然而,一种神经递质底物在睡眠-觉醒状态中介导呼吸肌的激活尚未被确定。Chan和同事(2)确定了舌下运动核内源性1-肾上腺素能受体机制在调节大鼠舌下肌活动中的作用。给大鼠植入电极以记录颏舌肌
Although the upper airway of children with obstructive sleep apnea (OSA) is more collapsible than in control subjects, most children with OSA experience prolonged periods of stable breathing at night. Both anatomic factors and the ability to mount a robust neuromuscular compensatory response to loading are important to the pathogenesis of OSA, with the latter particularly relevant to the ability to restore adequate airflow and sustain stable breathing. Accordingly, Katz and colleagues (1) determined the neuromuscular compensatory pharyngeal dilator muscle responses to airway collapsing pressures by recording genioglossus muscle activity in normal, healthy, sleeping children. The subjects (age range, 9.1–16.4 yr; mean, 11.9 yr; body mass index in the 70th percentile) were placed on 3 cm H2O of continuous positive airway pressure (CPAP), and mask pressure was then varied during sleep to a minimum of 22 cm H2O, with pressures applied for five consecutive breaths and returned to baseline for 30 seconds between interventions. There was wide intersubject variability in the magnitude of the genioglossus muscle responses to airway collapsing pressures in sleep. Importantly, the prominent increases in genioglossus activity in some subjects were associated with increased airflow during loading, increased respiratory rate, and decreased airflow resistance, and in some cases, recovery of normal ventilation without evidence of electrocortical arousal. The authors speculate that this robust pharyngeal dilator muscle response to loading may account for the periods of stable breathing during sleep in some children with OSA, and that the severity of sleep apnea for a given child is influenced by the balance between intrinsic anatomic factors (airway size and stiffness), neuromuscular compensatory responses to loading, and arousal threshold. The concept of a tonic drive activating respiratory muscles in wakefulness, but not sleep, has been an important and enduring notion in respiratory medicine, not least because it is the root mechanism to understand the effects of sleep on breathing and pathogenesis of sleep-related breathing disorders such as OSA. However, a neurotransmitter substrate that mediates activation of respiratory muscle across sleep–wake states had not been identified. Chan and colleagues (2) determined the role of endogenous 1-adrenergic receptor mechanisms at the hypoglossal motor nucleus in modulating genioglossus muscle activity in rats. The rats were implanted with electrodes to record genioglossus