Differential effects of clonidine on upper airway abductor and adductor muscle activity in awake goats

The purpose of this study was to determine the extent to which alpha(2)-adr enoceptor (alpha(2)-AR) pathways affect the central motor output to upper a irway muscles that regulate airflow. Electromyogram (EMG) measurements were made from posterior cricoarytenoid (PCA), cricothyroid (CT), thyroarytenoi d (TA), and middle (MPC) and inferior (IPC) pharyngeal constrictor muscles in awake standing goats. Systemic administration of the alpha(2)-AR agonist clonidine induced a highly dysrhythmic pattern of ventilation in all anima ls that was characterized by alternating episodes of tachypnea and slow irr egular breathing patterns, including prolonged and variable expiratory time intervals. Periods of apnea were commonly observed. Dysrhythmic ventilator y patterns induced by clonidine were associated with differential recruitme nt of upper airway muscles. alpha(2)-AR stimulation preferentially decrease d the activity of the PCA, CT, and IPC muscles while increasing TA and MPC EMG activities. Clonidine-induced apneas were associated with continuous to nic activation of laryngeal (TA) and pharyngeal (MPC) adductors, leading to airway closure and arterial oxygen desaturation. Tonic activation of the T A and MPC muscles was interrupted only during the first inspiratory efforts after central apnea. Laryngeal abductor, diaphragm, and transversus abdomi nis EMG activities were completely silenced during apneic events. Ventilato ry and EMG effects were reversed by selective alpha(2)-AR blockade with SKF -86466. The results demonstrate that alpha(2)-AR pathways are important mod ulators of central respiratory motor outputs to the upper airway muscles.