INCREASED VENOUS PCO(2) ENHANCES DYNAMIC-RESPONSES OF AVIAN INTRAPULMONARY CHEMORECEPTORS

We quantified the neural discharge of intrapulmonary chemoreceptors (I PC) innervating the left lungs of anesthetized Pekin ducks. Right and left lungs were separately unidirectionally ventilated. Alternating st eps in CO2 concentration (0-6%, 11-s period) were delivered to the lef t lung under control conditions [mixed venous Pco(2), (P $($) over bar $$ v(co2)) 43 +/- 4 Torr] and under venous CO2 load conditions (P $($) over bar$$ v(co2) 79 +/- 6 Torr). During venous CO2 loading the right lung was ventilated with 10-20% CO2, while the left lung was ventilat ed with a sufficient flow of gas containing 0% CO2 to maintain normal expired Pco(2) (indicated by constant IPC discharge rate). Venous load ing increased the peak-to-peak amplitude of the oscillation in IPC dis charge by 4.3 +/- 1.8 s(-1) (n = 11, P < 0.05), left lung ventilation was increased 2.6-fold, and the IPC step response became more prompt. The mean IPC discharge rate during the CO2 stepping cycle was not sign ificantly affected (11.8 +/- 1.4 during control vs. 10.3 +/- 1.3 s(-1) during venous loading). Increased IPC discharge oscillations were due to enhancement of the dynamic overshoot in receptor discharge after t he 6-0% downstep in inspired CO2 and to a depression of discharge duri ng 6% inspired CO2. We propose that the phasic enhancement of IPC disc harge oscillations during venous CO2 loading may cause feedback inhibi tion of ventilatory drive.