Cori Jennifer M, Thornton Therese, O'Donoghue Fergal J, Rochford Peter D, White David P, Trinder John, Jordan Amy S
Melbourne School of Psychological Sciences, University of Melbourne, Parkville, Victoria, Australia.
Institute for Breathing and Sleep and Austin Health, Heidelberg, Victoria, Australia.
Sleep. 2017 Jun 1;40(6). doi: 10.1093/sleep/zsx057.
To determine whether arousals that terminate obstructive events in obstructive sleep apnea (OSA) (1) induce hypocapnia and (2) subsequently reduce genioglossus muscle activity following the return to sleep.
Thirty-one untreated patients with OSA slept instrumented with sleep staging electrodes, nasal mask and pneumotachograph, end-tidal CO2 monitoring, and intramuscular genioglossus electrodes. End-tidal CO2 was monitored, and respiratory arousals were assigned an end-arousal CO2 change value (PETCO2 on the last arousal breath minus each individual's wakefulness PETCO2). This change value, in conjunction with the normal sleep related increase in PETCO2, was used to determine whether arousals induced hypocapnia and whether the end-arousal CO2 change was associated with genioglossus muscle activity on the breaths following the return to sleep.
Twenty-four participants provided 1137 usable arousals. Mean ± SD end-arousal CO2 change was -0.2 ± 2.4 mm Hg (below wakefulness) indicating hypocapnia typically developed during arousal. Following the return to sleep, genioglossus muscle activity did not fall below prearousal levels and was elevated for the first two breaths. End-arousal CO2 change and genioglossus muscle activity were negatively associated such that a 1 mm Hg decrease in end-arousal CO2 was associated with an ~2% increase in peak and tonic genioglossus muscle activity on the breaths following the return to sleep.
Arousal-induced hypocapnia did not result in reduced dilator muscle activity following return to sleep, and thus hypocapnia may not contribute to further obstructions via this mechanism. Elevated dilator muscle activity postarousal is likely driven by non-CO2-related stimuli.
确定阻塞性睡眠呼吸暂停（OSA）中终止阻塞性事件的觉醒是否（1）诱发低碳酸血症，以及（2）在重新入睡后是否随后降低颏舌肌活动。
31例未经治疗的OSA患者在睡眠时配备了睡眠分期电极、鼻罩和呼吸流速仪、呼气末二氧化碳监测仪以及颏舌肌肌内电极。监测呼气末二氧化碳，并为呼吸觉醒分配一个觉醒结束时的二氧化碳变化值（最后一次觉醒呼吸时的呼气末二氧化碳分压减去个体清醒时的呼气末二氧化碳分压）。该变化值，结合睡眠相关的呼气末二氧化碳分压正常升高，用于确定觉醒是否诱发低碳酸血症，以及觉醒结束时的二氧化碳变化是否与重新入睡后呼吸时的颏舌肌活动相关。
24名参与者提供了1137次可用的觉醒数据。觉醒结束时二氧化碳变化的平均值±标准差为-0.2±2.4 mmHg（低于清醒时），表明觉醒期间通常会出现低碳酸血症。重新入睡后，颏舌肌活动并未降至觉醒前水平以下，并且在前两次呼吸时升高。觉醒结束时的二氧化碳变化与颏舌肌活动呈负相关，即觉醒结束时二氧化碳分压每降低1 mmHg，重新入睡后呼吸时颏舌肌峰值和张力活动增加约2%。
觉醒诱发的低碳酸血症在重新入睡后并未导致扩张肌活动降低，因此低碳酸血症可能不会通过这种机制导致进一步的阻塞。觉醒后扩张肌活动升高可能由非二氧化碳相关刺激驱动。
