VOLUME-DEPENDENT APNEIC THRESHOLD DURING NREM SLEEP IN THE DOG

We determined the causes of central apnea that commonly follow the hyp erpnea resulting from brief airway occlusion during non-rapid-eye-move ment (NREM) sleep. Ventilation and end-tidal gases were measured befor e, during, and after 214 trials of 15-20 s of tracheal occlusion in th ree dogs during NREM sleep. Airway occlusion was accompanied by progre ssive increases in inspiratory effort and was followed by transient on e- to four-breath hyperpneas, with subsequent central apnea [3-15 time s eupneic control expiratory duration (TE)] in 62% of occlusion trials . Significant TE prolongation after hyperventilation did not occur unt il tidal volume (VT) was three times greater than control; i.e., there was a volume-dependent apneic threshold. Transient electroencephalogr am arousal at the end of the occlusion often augmented VT, thereby con tributing to the subsequent central apnea; however, arousal was not re quired for the apnea to occur. Significant transient hypocapnia (up to -12 Torr arterial PCO2) commonly occurred after release of airway occ lusion but was not closely correlated with the length of central apnea . During vagal blockade, after release of airway occlusion, significan t transient hyperventilation occurred but at VT < 40% greater than con trol, and TE prolongation was markedly reduced. In summary, after rele ase of airway occlusion in NREM sleep, 1) VT greater than three times eupnea was necessary to cause central apnea, 2) transient arousal at t he termination of airway occlusion caused longer apneas by augmenting VT, and 3) transient hypocapnia per se made a significant but minor co ntribution to the postocclusion central apnea.