EVIDENCE FOR A CENTRAL ACTION OF CO2 VENTILATORY STIMULUS IN PEKIN DUCKS

Abstract

Ventilatory responses to changes in PCO2 [CO2 partial pressure] of the blood perfusing the central nervous system were studied breath by breath by pneumotachography in Pekin ducks under transient and steady conditions. In conscious birds all the arteries to the cephalic region were tied or clamped, except the right internal carotid. The blood supply via the single remaining arterial pathway was transiently replaced, for about 15 s, by injecting 2 ml of blood previously made normocapnic (control; PCO2 = 32 torr) or hypercapnic (test; PCO2 = 76 torr) from a syringe thermostated at 41.degree. C, under normal oxygenation (PO2 [O2 partial pressure] around 110 torr) and mean endovascular pressure (107 mm Hg). During control injections no significant ventilatory changes were observed. Test injections provoked an early and significant 20% increase in the minute volume of ventilation. Using cross-perfusion between pairs of anesthetized ducks, the head of a recipient animal (R) was vascularly isolated from the trunk and perfused by a donor (D), the nervous connections with the trunk remaining intact. When giving some CO2 to breathe to D (FICO2 [inspired CO2 fraction] = 0.05) while R breathed ambient air, arterial PCO2 increased in D and in the head of R, and hyperventilation occurred in both ducks. As a consequence of this hyperventilation, PCO2 decreased in the arterial blood and the end-tidal gas of R. There is a central action of CO2 as a ventilatory stimulus in ducks.