Abstract
In 11 cats anaesthetized with chloralose-urethane, the steady state ventilation during hyperoxia was measured as a function of the central Pa CO 2 (Pa CO 2 c) and peripherial Pa CO 2 (Pa CO 2 p) using the technique of artificial ponto-medullary perfusion. The ventilatory response was described by V ̇ e = Sc·Pa CO 2 c + Sp·Pa CO 2 p − K where Sc and Sp represent the overall central and peripheral sensitivity to carbon dioxide. The posthyperventilation apnoeic threshold values of Pa CO 2 p for several fixed values of Pa CO 2 c were also assessed. It was found that down to Pa CO 2 c's of about 3.5 kPa (26 mm Hg) the response surface for spontaneous ventilation could be used to satisfactorily predict the Pa CO 2 p as a function of Pa CO 2 c at apnoea. In 4 cats the ventilatory response to changes in centra P CO 2 was measured after carotid body denervation. These response curves were linear down to the P CO 2 -axis. We conclude that in anaesthetized cats during hyperoxia: (1) the above equation for the ventilation appears to be valid down to CO 2 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 CO 2 response curve is linear down to ventilation zero; (4) the Pa CO 2 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.
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