上气道扩张肌功能障碍目前被认为是阻塞性睡眠呼吸暂停低通气综合征（OSAHS）核心的发生机制。上气道扩张肌的激活，对于维持睡眠时气道的开放起重要作用。睡眠呼吸暂停发生时呼吸驱动下降，造成上气道扩张肌张力和咽腔负压平衡出现失调。研究提示，咽腔内压力变化的刺激可以通过呼吸中枢对上气道扩张肌进行反馈调控。说明咽腔粘膜的感觉传入功能可能与OSAHS神经肌肉方面的发病机制相关。为证实该假设，本研究在既往研究的基础上，通过定量改变咽腔内部压力，观察睡眠时颏舌肌肌电的变化规律，了解咽部压力刺激变化对上气道扩张肌功能的影响。并进一步在动物模型上，观察不同咽腔压力下颏舌肌肌电在咽部粘膜表面麻醉与非麻醉阻滞组之间的差异，阐明咽腔粘膜感受器在上气道扩张肌活性调控中的作用。阐明上述问题将为深入认识OSAHS神经肌肉调控机制，寻找新的治疗靶点提供理论依据。

The key pathogenesis of obstructive sleep apnea-hypopnea syndrome (OSAHS) are now recognized as upper airway(UA) dilators dysfunction. The activation of the UA dilators may play an important role to restore pharyngeal patency. Sleep apnea occurs during the low respiratory drive period, and the balance of UA dilators activity and pharyngeal airway negative pressure appears disorders. Recent studies confirmed that the UA dilators can be regulated by the activation of the respiratory drive center via the sensory afferent pathway initiated by the change of pharyngeal pressure. It is believed that the afferent function of pharyngeal mucosa may be closely related to the neuromuscular pathogenesis of OSAHS. Based on the previous studies, we want to observe the variation of genioglossus electromyography following alteration of upper airway pressure to make sure the effects of pharyngeal pressure on genioglossus activity. Further to observe genioglossus activity under different negative airway pressure in animal model with or without mucosa anaesthesia blocked, in order to clarify the role of pharyngeal mucosa receptor in the pathway of genioglossus feedback control. Clarifying these issues could help us to get in-depth understanding of OSAHS neuromuscular control mechanism and provide a theoretical basis for new therapeutic options.