Hypoxia and hypercapnia as respiratory stimulants and depressants

The effect of wide variations in arterial O₂ and CO₂ tensions on phrenic nerve activity was evaluated in anesthetized dogs which were paralyzed so that the physical properties of the lung and chest wall could not influence respiratory neuron response. The techniques used allowed the effects of hypoxia and hypercapnia to be assessed either separately or in combination. The results showed that hypoxia enhanced the stimulating effects of hypercapnia on respiratory neuron response by (1) decreasing the arterial CO₂ tension at which phasic phrenic activity begins and by (2) increasing the change in phrenic nerve activity produced by a given rise in arterial CO₂ tension. However, hypoxia also augmented the depressing effect of hypercapnia by (1) decreasing the arterial CO₂ tension at which peak phrenic nerve activity occurred and by (2) reducing the range of arterial CO₂ tensions over which progressive hypercapnia increased phrenic nerve activity. The results suggest that the usual steady state methods of evaluating hypoxic response may be measuring opposing effects of hypoxia on ventilation; a stimulating effect of hypoxia at the peripheral chemoreceptor; and a depressing central effect of hypoxia.