NEUROMUSCULAR ACTIVITY AND UPPER AIRWAY COLLAPSIBILITY - MECHANISMS OF ACTION IN THE DECEREBRATE CAT

We have shown that tracheal and tongue displacement represent two basi c mechanisms by which upper airway collapsibility can be altered. In t his study, we investigated whether hypercapnia, which activates upper airway muscles, alters upper airway collapsibility by a mechanism simi lar to tracheal or tongue displacement. To answer this question, we ut ilized a feline isolated upper airway preparation in which maximal ins piratory airflow ((V) over dot imax), the pharyngeal critical pressure (Pcrit) and the nasal resistance (Rn) upstream to the flow-limiting s ite (FLS) were measured. In protocol #1, upper airway airflow dynamics were studied at two levels of trachea displacement under either hypo- or hypercapnic conditions. We found that the increase in (V) over dot imax with 1 cm of caudal tracheal displacement was attenuated by hyper capnia (44 +/- 12 ml/s versus 81 +/- 7 ml/s during hypocapnia, p 0.048 ), as was the decrease in Pcrit (-2.4 +/- 1.1 cm H2O versus -5.2 +/- 1 .1 cm H2O, p = 0.001). In protocol #2, we investigated the effect of t ransecting the cervical strap muscles and hypoglossal nerves on airflo w dynamics during hypercapnia. (V) over dot imax, Pcrit, and Rn did no t change after transecting either the strap muscles or the hypoglossal nerves. We conclude that the primary mechanism for changes in Pcrit d uring hypercapnia is similar to trachea displacement and is mediated b y muscles other than the straps or tongue.