The role of the vagus nerves in the ventilatory response to loweredP a O2 with intact and eliminated carotid chemoreflexes

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Abstract
In anaesthetized rabbits the influence of vagal cold-block on the ventilatory response to lowered arterial oxygen pressure was investigated. With intact carotid chemoreflexes, loweredP a O2 caused hyperventilation, which was progressively intensified with the degree of hypoxia, regardless of whether the alveolarPCO2 was uncontrolled or kept constant at the hyperoxic control. The “P a O2” response was to a greater extend due to an increase of respiratory rate than to one of tidal volume. During hyperoxia, vagal cold-block caused a distinct increase in ventilation provided the alveolarPCO2 was not allowed to decrease. During moderate hypoxia, vagal block caused only a slight increase in ventilation, whenP A CO2 was not controlled, but a distinct decrease in ventilation, whenP A CO2 was maintained at the hyperoxic level. Without carotid chemoreflexes, loweredP a O2 did not change ventilation at any level, provided the vagus nerves were left intact. This was due to a substantial increase in respiratory rate counteracting a corresponding decrease in tidal volume. Then vagal block led to a ventilatory depression depending on the degree of hypoxia, which was due to a simultaneous decline in respiratory rate and tidal volume. It is concluded that during hypocapnic hypoxia the vagal stretch reflex primarily inhibits the carotid chemoreflex drive of ventilation. During normocapnic hypoxia, however, the mode of interaction between the peripheral and the central chemical drive has to be considered, which without vagal feed-back is occlusive. This occlusion appears to be counteracted by a vagal mechanism sensitive to CO2 in the airways — and possibly also to a lack of O2 —, mainly shortening respiratory cycle duration.