Interaction of hypercapnia and phasic volume feedback on motor control of the upper airway.

The effect of hypercapnia on the suppression of efferent hypoglossal and recurrent laryngeal nerve activity by phasic volume feedback was studied in decerebrate paralyzed intubated cats ventilated with a phrenic-driven servo-respirator. The gain of the respirator was altered for single inspirations, and the resulting changes in neural activities were quantified by comparison with respective neural activities without phasic volume feedback. This maneuver was performed when the end-tidal CO2 concentration was 5, 7, and 9%. Changes in the level of CO2 did not alter the slope or position of the volume thresholds for suppression of hypoglossal and recurrent laryngeal activities. The slope of the volume-time isopleths for specific levels of graded suppression also remained constant for each nerve at the different levels of CO2. Under hypercapnic conditions, greater volumes were required at a given time into inspiration to achieve any particular level of suppression, but these differences generally did not reach statistical significance. These data demonstrate a lack of effect of the CO2 stimulus on the suppression of upper airway motoneuron activity by phasic volume feedback. Despite the absence of this interaction, a CO2-induced increase in central inspiratory activation of upper airway motoneurons, in the presence of a very sensitive volume feedback system, would help maintain airway patency in the face of upper airway narrowing or closure.