Ventilatory response to carbon dioxide and apnoeic thresholds.

In 11 cats anaesthetized with chloralose-urethane, the steady state ventilation during hyperoxia was measured as a function of the central PaCO2 (PacCO2) and peripheral PaCO2 (PapCO2) using the technique of artificial ponto-medullary perfusion. The ventilatory response was described by VE = Sc . PacCO2 + Sp . PapCO2 - K where Sc and Sp represent the overall central and peripheral sensitivity to carbon dioxide. The post-hyperventilation apnoeic threshold values of PapCO2 for several fixed values of PacCO2 were also assessed. It was found that down to PaCCO2's and PapCO2's of about 3.5 kPa (26 mm Hg) the response surface for spontaneous ventilation could be used to satisfactorily predict the PapCO2 as a function of PacCO2 at apnoea. In 4 cats the ventilatory response to changes in central PCO2 was measured after carotid body denervation. These response curves were linear down to the PCO2-axis. We conclude that in anaesthetized cats during hyperoxia: (1) the above equation for the ventilation appears to be valid down to CO2 tensions of about 3.5 kPa (26 mm Hg); (2) the peripheral and central chemoreceptors exhibit neural activity down to at least 2.0 kPa (15 mm Hg); (3) in non-artificially perfused cats the CO2 response curve is linear down to ventilation zero; (4) the PaCO2 at apnoea (apnoeic 'threshold') in non-artificially perfused cats does not constitute a neural threshold for the peripheral or for the central chemoreceptors. Using these results a respiratory controller equation is proposed and some possible implications for the neural organization of the respiratory controller are discussed.