Differential inhibition of the diaphragm and posterior cricoarytenoid muscles induced by transient hypertension across sleep states in intact cats.

Arterial pressure was transiently elevated by intravenous infusion of phenylephrine in intact, freely moving cats during sleep and waking states to determine pressure effects on diaphragmatic and laryngeal abductor EMG activity. Transient hypertension caused respiratory cycle duration to increase and integrated EMG area to decrease for several breaths in both the diaphragm and posterior cricoarytenoid, the integrated inspiratory area of which decreased to a greater extent than did that of the diaphragm. Cycle duration increases resulted from increases in expiratory duration. Expiratory duration of the posterior cricoarytenoid initially increased proportionately more than that of the diaphragm, causing a transient phase disassociation between that upper airway muscle and diaphragmatic timing. This disassociation disappeared after several breaths. Changes in posterior cricoarytenoid expiratory duration and integrated inspiratory area were sleep state-dependent: area decreases were greatest in rapid eye movement sleep; expiratory duration increases were greatest in quiet sleep. Neural mechanisms underlying laryngeal abductor activity are sleep state-dependent and appear to be affected more than diaphragmatic mechanisms by baroreceptor stimulation.