Bellemare François, Pecchiari Matteo, Bandini Monica, Sawan Mohamad, D'Angelo Edgardo
Laboratoire du sommeil, Service de pneumologie, Centre Hospitalier de l'Université de Montréal, Hôtel-Dieu, Montréal, Quebec, H2W 1T8 Canada.
Am J Respir Crit Care Med. 2005 Sep 1;172(5):606-12. doi: 10.1164/rccm.200502-190OC. Epub 2005 Jun 9.
Anesthesia-induced uncoupling of upper airway dilating and inspiratory pump muscles activation may cause inspiratory flow limitation, thereby mimicking obstructive sleep apnea/hypopnea.
Determine whether inspiratory flow limitation occurs in spontaneously breathing anesthetized rabbits and whether this can be reversed by direct hypoglossal nerve stimulation and by the application of continuous positive airway pressure.
Ten New Zealand White rabbits were anesthetized, instrumented, and studied supine while breathing spontaneously at ambient pressure or during the application of positive or negative airway pressure. Under each of these conditions, the effect of unilateral or bilateral hypoglossal nerve stimulation was investigated.
Inspiratory flow and tidal volume were measured together with esophageal pressure and the electromyographic activity of diaphragm, alae nasi, and genioglossus muscles.
Anesthesia caused a marked increase in inspiratory resistance, snoring, and in eight rabbits, inspiratory flow limitation. Hypoglossus nerve stimulation was as effective as continuous positive airway pressure in reversing inspiratory flow limitation and snoring. Its effectiveness increased progressively as airway opening pressure was lowered, reached a maximum at -5 cm H2O, but declined markedly at lower pressures. With negative airway opening pressure, airway collapse eventually occurred during inspiration that could be prevented by hypoglossus nerve stimulation. The recruitment characteristics of hypoglossus nerve fibers was steep, and significant upper airway dilating effects already obtained with stimulus intensities 36 to 60% of maximum.
This study supports hypoglossus nerve stimulation as a treatment option for obstructive sleep apnea.
麻醉诱导的上气道扩张肌与吸气泵肌激活的解耦可能导致吸气气流受限，从而模拟阻塞性睡眠呼吸暂停/低通气。
确定在自主呼吸的麻醉兔中是否会出现吸气气流受限，以及直接舌下神经刺激和应用持续气道正压通气能否逆转这种情况。
10只新西兰白兔麻醉后进行仪器安装，在常压下自主呼吸或应用正压或负压气道通气时仰卧位进行研究。在每种情况下，研究单侧或双侧舌下神经刺激的效果。
测量吸气气流、潮气量、食管压力以及膈肌、鼻翼肌和颏舌肌的肌电图活动。
麻醉导致吸气阻力显著增加、打鼾，8只兔子出现吸气气流受限。舌下神经刺激在逆转吸气气流受限和打鼾方面与持续气道正压通气同样有效。随着气道开放压力降低，其有效性逐渐增加，在-5 cm H₂O时达到最大值，但在更低压力下显著下降。在负气道开放压力下，吸气时最终会发生气道塌陷，而舌下神经刺激可预防这种情况。舌下神经纤维的募集特征陡峭，刺激强度达到最大值的36%至60%时就已获得显著的上气道扩张效果。
本研究支持舌下神经刺激作为阻塞性睡眠呼吸暂停的一种治疗选择。
