Ventilatory control during brief infusions of CO₂ laden blood in the awake dog

CO₂ equilibrated blood was briefly infused at constant rates into the ascending aorta (AA) and superior vena cava (SVC) of unanesthetized dogs and the ventilatory responses (VE, VT, f) determined breath by breath. Responses to SVC infusions did not begin until the infused stimulus reached the systemic arterial circulation. Responses to AA infusion had an average latency of 6.6 sec and a peak response time of 18.6 sec. A linear relationship was found between peak VE and PaCO₂ with slope (S) = 0.58 liter/min per mm Hg. VE increased with stimuli as small as 1 mm Hg Δ PaCO₂. Pentobarbital markedly depressed ventilatory responses. Bilateral carotid body resection (CBR) doubled latency but did not affect peak response time or S. When CBR animals were vagotomized, peak response time and S remained unaltered and latency was not further changed. The duration of response, however, was significantly prolonged. These results demonstrate the presence of a ventilatory control component capable of triggering rapid changes in ventilation in response to brief, 'physiologic' changes in arterial PCO₂ and pH. The carotid and aortic bodies proved not to be the unique chemoreceptors responsible for these rapid responses.