Hypoxemic threshold for lung ventilation in the toad

The relationship between the buccal force pump, expressed as the time internal of positive buccal pressure, and Pa O 2 was investigated in conscious toads, Bufo marinos, unidirectionally ventilated at a high flow rate (240–260 ml/min). The high ventilatory flow rate meant that Pa O 2 was largely independent of the animal's ventilatory activity so that the relationship between pulmonary ventilation and Pa O 2 was effectively open-loop. The hypoxemic threshold (Pa O 2 ) for lung ventilation was 54.2 mm Hg in hypocapnia (Pa CO 2 = 4.7 ± 0.3 mm Hg), 82.6 mm Hg in normocapnia (Pa CO 2 = 11.6 ± 0.2 mm Hg), and 137.9 mm Hg in hypercapnia (Pa CO 2 = 20.1 ± 0.1 mm Hg). Unidirectional ventilation with 20% O 2 in N 2, a condition in which the toads were normoxic but hypocapnic, stopped pulmonary ventilation cycles. Taken with existing evidence that hyperoxia stops pulmonary ventilation even under conditions in which Pa CO 2 is elevated, this suggests that hypoxic and hypercapnic stimuli summate to drive lung ventilation in the toad. Bilateral denervation of the carotid labyrinths decreased pulmonary ventilation in absolute terms, but did not reduce the proportionate increase in pulmonary ventilation in response to normocapnic hypoxia, suggesting the chemoreceptors within the carotid labyrinth may contribute to, but are not solely responsible for, the hypoxemic ventilatory drive.