We hypothesized that CO2, like hypoxia and withdrawal of pulmonary slo
wly adapting receptor input, would cause tracheal constriction during
neural apnea (absence of phrenic activity). In seven anesthetized para
lyzed dogs ventilated to neural apnea, we increased arterial Pco(2) (P
a-CO2) in steps by adding CO2 to the inspirate while keeping ventilati
on constant. Increases in Pa-CO2 caused tracheal constriction during n
eural apnea in all dogs; 69 +/- 26 (SD)% of the change in tracheal dia
meter occurred during neural apnea. Average sensitivity of tracheal di
ameter to CO2 was 0.44 mm/Torr Pa-CO2. Our data suggest that central c
hemoreceptor inputs to brain stem neurons controlling smooth muscle of
the extrathoracic airway bypass central mechanisms generating inspira
tion.