Clonidine induces upper airway closure in awake goats

We examined the effects of the alpha(2)-adrenoceptor (alpha(2)-AR) agonist clonidine on pressure-flow relationships in the upper airway. Inspired and expired airflows, subglottic tracheal pressure (PTR), mask pressure and mid dle pharyngeal constrictor (MPC) and diaphragm electromyogram (EMG) activit ies were recorded in awake standing goats. Clonidine-induced central apneas were always associated with continuous tonic activation of the MPC. Subglo ttic PTR during expiration increased progressively in a dose-dependent mann er after clonidine administration. In all cases, positive subglottic PTR wa s maintained throughout the duration of clonidine-induced apneas and was su fficient to retard or prevent expiratory flow during early and mid-expirati on indicating complete airway closure. The effects of clonidine were revers ed by selective alpha(2)-AR blockade with SKF-86466. Central apneas after s pontaneous augmented breaths (sighs) were associated with continuous tonic activation of the MPC throughout the duration of the prolonged TE intervals . However, subglottic PTR during expiration was not significantly different from control breaths and there was no evidence of increased expiratory air way resistance or delayed expiratory flow. We conclude that continuous toni c activation of pharyngeal adductor muscles appears to be a constant featur e of central apnea in the awake goat independent of the initiating cause of the apnea. However, our data suggest that MPC activation alone may not be sufficient to cause complete closure of the upper airway during central apn ea. (C) 2000 Elsevier Science B.V. All rights reserved.