Negative pressure-induced deformation of the upper airway causes central apnea in awake and sleeping dogs.

We investigated the effects of negative pressure (NP) in the isolated upper airway (UA) in three unanesthetized dogs. The UA was isolated, and the dogs breathed through an endotracheal tube while wearing a fitted fiberglass snout mask. NP (-2 to -32 cmH2O) was applied in a square wave below the larynx or at the snout at end expiration and was held until inspiratory effort during wakefulness, non-rapid-eye-movement (NREM) sleep, and rapid-eye-movement (REM) sleep. During all states of consciousness, NP applied to the UA prolonged expiratory time (TE) 1) below a threshold of -8 to -10 cmH2O, which coincided with closure of the oro- and/or velopharynx; and 2) in a progressive fashion at more negative pressures than threshold, up to a mean apneic length of 324% of the control value (or 13.9 s) at -30 cmH2O. TE prolongation was less during REM sleep at a given NP (P < 0.05). Augmented tonic genioglossal electromyographic activity also occurred with the applied NP during wakefulness and NREM sleep but not with REM sleep. NP (-20 to -32 cmH2O) applied as a brief pulse (300-500 ms) during NREM sleep caused transient airway occlusion, terminated the breath during inspiration, and prolonged TE when applied at end expiration. Central apneas always persisted beyond the termination of the UA closure. TE prolongation in response to NP persisted in the presence of a topical anesthetic nebulized through the UA sufficient to abolish the laryngeal gag reflexes. We conclude that UA closure and deformation will cause significant TE prolongation during all states of consciousness and activation of the genioglossus muscle during wakefulness and NREM sleep but not during REM sleep.