VOLUME-DEPENDENT APNEIC THRESHOLD DURING NREM SLEEP IN THE DOG
VOLUME-DEPENDENT APNEIC THRESHOLD DURING NREM SLEEP IN THE DOG
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DOI：
10.1152/jappl.1994.76.6.2315
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发表时间：
1994-06-01
影响因子：
3.3
通讯作者：
DEMPSEY, JA
中科院分区：
文献类型：
--
作者：
CHOW, CM;XI, L;DEMPSEY, JA
我们确定了中枢性呼吸暂停的原因，这些呼吸暂停通常伴随着非快速眼动(NREM)睡眠期间短暂的呼吸道阻塞引起的高呼吸暂停。对3只犬在非快速眼动睡眠期进行了15-20次S气管阻断试验，分别在试验前、试验中和试验后测定了通气量和呼气末气体浓度。在62%的阻塞试验中，呼吸道阻塞伴随着吸气努力的进行性增加，紧随其后的是一过性一到四次呼吸过多，随后出现中枢性呼吸暂停[3-15倍正常对照呼气持续时间(TE)]。过度换气后，直到潮气量(VT)大于对照组的3倍时，TE才显著延长，即存在容量依赖的呼吸暂停阈值。在闭塞结束时，短暂的脑电唤醒通常会增加室速，从而导致随后的中枢性呼吸暂停；然而，觉醒并不是发生呼吸暂停所必需的。显著的一过性低碳酸血症(高达-12托动脉二氧化碳分压)通常发生在解除呼吸道阻塞后，但与中枢性呼吸暂停的长度并不密切相关。迷走神经阻断期间，在解除气道阻塞后，出现了明显的一过性过度换气，但在VT和Lt；时比对照组大40%，TE延长明显减少。综上所述，在NREM睡眠状态下解除呼吸道阻塞后，1)VT大于3倍Eupnea是导致中枢性呼吸暂停的必要条件，2)气道阻塞终止时的一过性觉醒通过增加VT而导致较长的呼吸暂停，3)短暂低碳酸血症本身对阻塞后的中枢性呼吸暂停有显著但轻微的贡献。
We determined the causes of central apnea that commonly follow the hyperpnea resulting from brief airway occlusion during non-rapid-eye-movement (NREM) sleep. Ventilation and end-tidal gases were measured before, during, and after 214 trials of 15-20 s of tracheal occlusion in three dogs during NREM sleep. Airway occlusion was accompanied by progressive increases in inspiratory effort and was followed by transient one- to four-breath hyperpneas, with subsequent central apnea [3-15 times eupneic control expiratory duration (TE)] in 62% of occlusion trials. Significant TE prolongation after hyperventilation did not occur until tidal volume (VT) was three times greater than control; i.e., there was a volume-dependent apneic threshold. Transient electroencephalogram arousal at the end of the occlusion often augmented VT, thereby contributing to the subsequent central apnea; however, arousal was not required for the apnea to occur. Significant transient hypocapnia (up to -12 Torr arterial PCO2) commonly occurred after release of airway occlusion but was not closely correlated with the length of central apnea. During vagal blockade, after release of airway occlusion, significant transient hyperventilation occurred but at VT < 40% greater than control, and TE prolongation was markedly reduced. In summary, after release of airway occlusion in NREM sleep, 1) VT greater than three times eupnea was necessary to cause central apnea, 2) transient arousal at the termination of airway occlusion caused longer apneas by augmenting VT, and 3) transient hypocapnia per se made a significant but minor contribution to the postocclusion central apnea.