Neuromuscular Activity and Upper Airway Collapsibility

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Abstract
We have shown that tracheal and tongue displacement represent two basic mechanisms by which upper airway collapsibility can be altered. In this study, we investigated whether hypercapnia, which activates upper airway muscles, alters upper airway collapsibility by a mechanism similar to tracheal or tongue displacement. To answer this question, we utilized a feline isolated upper airway preparation in which maximal inspiratory airflow (Vimax), the pharyngeal critical pressure (Pcrit) and the nasal resistance (Rn) upstream to the flow-limiting site (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 Vimax with 1 cm of caudal tracheal displacement was attenuated by hypercapnia (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 transecting the cervical strap muscles and hypoglossal nerves on airflow dynamics during hypercapnia. Vimax, Pcrit, and Rn did not change after transecting either the strap muscles or the hypoglossal nerves. We conclude that the primary mechanism for changes in Pcrit during hypercapnia is similar to trachea displacement and is mediated by muscles other than the straps or tongue.