Abstract
The steady-state stimulus-response relations between arterial pq, and P CO 2 , and the mean activity of carotid chemoreceptors (single and multi-fiber) and ventilation were simultaneously recorded in 48 anesthetized cats. The carotid chemoreceptor activity varied linearly with the increase of arterial P CO 2 , below and above the normal value, at any given level of arterial P O 2 . A decrease in arterial Po, increased the activity of the carotid chemoreceptors and increased its sensitivity to changes in arterial P CO 2 showing multiplicative stimulus interaction. The authors also found that the response in ventilation during hypoxia to changes in arterial P CO 2 , below the normal value was smaller than that to changes above it, unlike the response of carotid chemoreceptors. This arterial P CO 2 , quasi-threshold for ventilation was, therefore, not due to a corresponding threshold for the activity of the carotid chemoreceptors but to a central mechanism. Above the central Pa CO 2 threshold, the ventilatory response to changes in Pa CO 2 , and Pa O 2 resembled that of chemoreceptors but the ventilation dependent on hypoxia was greater than that could be directly accounted for by the activity of peripheral chemoreceptors. A multiplicative interaction between the activity of peripheral chemoreceptors and central CO 2 excitation appears to play a role in the regulation of ventilation.
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