Abstract

In conscious intact cats, oxygen breathing for up to 1 h does not modify ventilation, and the ventilatory response to CO 2 in hyperoxia is not consistently decreased. However, oxygen breathing induces sustained hyperventilation in conscious cats after carotid body denervation. In anesthetized ctas, oxygen breathing provokes a hypoventillation which is transient under light anesthesis but more sustained under deeper levels of anesthesia. At all levels of anesthesia, the ventilatory response to CO 2 is decreased in hyperoxia as compared with normaxia. These results suggest that: (1) the effects of hyperoxia include a central stimulating component, seen only in conscious animals, which offsets the decreased ventilatory drive from peripheral chemoreceptors; (2) this central component is sensitive to anesthesia, thus allowing an explanation for the permanent decrease in ventilation and decrease in ventilatory response to CO 2 observed when oxygen is given during deep anesthesia; and (3) anesthesia may help to purposefully unmask factors involved in the control of breathing, but it markedly alters the normal functioning of the respiratory network.

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