Am. J. Respir. Crit. Care Med., Volume 156, Number 2, August 1997, 515-521

Neuromuscular Activity and Upper Airway Collapsibility
Mechanisms of Action in the Decerebrate Cat

JAMES A. ROWLEY, BERNESTA C. WILLIAMS, PHILIP L. SMITH, and ALAN R. SCHWARTZ

Division of Pulmonary and Critical Care Medicine, Department of Medicine, The Johns Hopkins Medical Institutions, Baltimore, Maryland

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 ( Imax), 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 Imax 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. Imax, 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.

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