Sleep Center, Foothills Medical Centre, University of Calgary, Calgary, Alberta, Canada.
Sleep. 2011 Aug 1;34(8):1061-73. doi: 10.5665/SLEEP.1162.
Subjects with a collapsible upper airway must activate their pharyngeal dilators sufficiently in response to increasing chemical drive if they are to maintain airway patency without arousal from sleep. Little is known about the response of pharyngeal dilators to increasing chemical drive in these subjects. We wished to determine, in obstructive apnea patients, the response of the genioglossus to increasing chemical drive and the contribution of mechanoreceptor feedback to this response.
Physiological study.
University-based sleep laboratory.
20 patients with obstructive apnea.
Genioglossus activity was monitored during overnight polysomnography on optimal continuous positive airway pressure (CPAP). Intermittently, inspired gases were altered to produce different levels of ventilatory stimulation. CPAP was then briefly reduced to 1.0 cm H(2)O (dial-down), inducing an obstruction.
Without mechanoreceptor feedback (i.e., on CPAP) the increase in genioglossus activity as ventilation increased from 6.1 ± 1.4 to 16.1 ± 4.8 L/min was modest (ΔTonic activity 0.3% ± 0.5%maximum; ΔPhasic activity 1.7% ± 3.4%maximum). Genioglossus activity increased immediately upon dial-down, reflecting mechanoreceptor feedback, but only when ventilation before dial-down exceeded a threshold value. This threshold varied among patients and, once surpassed, genioglossus activity increased briskly with further increases in chemical drive (1.1% ± 0.84%GG(MAX) per L/min increase in V(E)).
In sleeping obstructive apnea patients: (1) Mechanoreceptor feedback is responsible for most of the genioglossus response to chemical drive. (2) Mechanoreceptor feedback is effective only above a threshold chemical drive, which varies greatly among patients. These findings account in part for the highly variable relation between pharyngeal mechanical abnormalities and apnea severity.
如果具有可塌陷上气道的受试者要在睡眠中不因觉醒而保持气道通畅，那么他们必须对上气道扩张肌施以足够的刺激以响应逐渐增加的化学驱动。对于这些患者，有关上气道扩张肌对逐渐增加的化学驱动的反应，人们知之甚少。我们试图在阻塞性睡眠呼吸暂停患者中确定颏舌肌对增加的化学驱动的反应，以及机械感受器反馈对这种反应的贡献。
生理学研究。
以大学为基础的睡眠实验室。
20 例阻塞性睡眠呼吸暂停患者。
在最佳持续气道正压通气（CPAP）的整夜多导睡眠图监测颏舌肌活动。间歇性地，改变吸入气体以产生不同水平的通气刺激。然后，CPAP 短暂降低至 1.0 cm H₂O（降档），诱发阻塞。
在没有机械感受器反馈（即在 CPAP 时）的情况下，通气从 6.1 ± 1.4 增加到 16.1 ± 4.8 L/min 时，颏舌肌活动的增加幅度较小（紧张性活动增加 0.3% ± 0.5%最大；相位性活动增加 1.7% ± 3.4%最大）。降档后，颏舌肌活动立即增加，反映了机械感受器反馈，但仅当降档前的通气超过阈值时才会增加。该阈值在患者之间存在差异，一旦超过，颏舌肌活动随着化学驱动的进一步增加而迅速增加（V(E)每增加 1 L/min，颏舌肌活动增加 1.1% ± 0.84%GG(MAX)）。
在睡眠中的阻塞性睡眠呼吸暂停患者中：（1）机械感受器反馈是颏舌肌对化学驱动的大部分反应的原因。（2）机械感受器反馈仅在阈值化学驱动以上有效，而该阈值在患者之间差异很大。这些发现部分解释了咽腔机械异常与呼吸暂停严重程度之间高度可变的关系。
