Ventilatory responses to carbon dioxide inhalation after vagotomy in chickens.

Both vagus nerves in 7 anesthetized chickens were cut midcervically. Inspired PCO2 was increased from 0 to 28 torr by successive 3.5 or 7 torr increments and then increased directly to 70 torr. At each level of PICO2, steady-state measures of PaCO2, [H+]a, VT, f and VE were made. When PICO2 was raised to 7 torr, PaCO2 AND [H+]a were above their control levels (i.e. PICO2 = 0); at each successive level of PICO2, both PaCO2 and [H+]a increased. Minute volume increased at 28 torr PICO2 but changes in VT and f individually were not significant. At 70 torr PICO2, VE and VT increased but f was not changed from its control value. We have previously suggested that CO2-sensitive intrapulmonary chemoreceptors mediate the arterial isocapnic hyperpnea at low PICO2 in chickens. The observation that vagotomy abolishes regulation of PaCO2 at low PICO2 is consistent with this hypothesis, since the afferent pathway of avian intrapulmonary chemoreceptors is predominantly vagal.