Key result
In unanaesthetized Bufo paracnemis, reductions in arterial PO2 stimulated ventilation, whereas carboxyhaemoglobinaemia per se failed to increase ventilation when pH was compensated.
In Bufo paracnemis, O2 partial pressure provides the principal O2 stimulus to breathe, rather than arterial O2 content.
PO2, not O2 content, drives ventilation in this amphibian; leaves open chemoreflex mechanisms in mammals.
The modality of the O2 drive to breathe was evaluated in unanaesthetized Bufo paracnemis. Carbon monoxide (CO) hypoxia was applied to reduce CaO2 (arterial O2 content). Arterial PO2 (PaO2) was reduced through inspiration of hypoxic gas mixtures (hypoxic hypoxia). Measurements included pulmonary ventilation, CaO2, PaO2, pHa, blood pressure and heart rate. Application of fractional concentrations of CO equivalent to 0.001 reduced CaO2 from 11.6 +/- 1.2 to 8.6 +/- 0.7 vol% (mean +/- S.E.M., N = 6) without any effect on heart rate, blood pressure or ventilation. Inspiration of fractional concentrations of CO equivalent to 0.01 reduced CaO2 to 5.1 +/- 0.7 vol%, which was accompanied by increased ventilation. This response, however, correlated with a decreased arterial pH. The effect of a fractional concentration of CO of 0.01 on ventilation was abolished by compensation of pH through bicarbonate infusion. Consequently, carboxyhaemoglobinaemia per se failed to increase ventilation. By contrast, reductions of PaO2 clearly stimulated ventilation, which indicates that O2 partial pressure provides the principal O2 stimulus to breathe in Bufo paracnemis.
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Branco et al. (1995) studied this question. Carbon monoxide (CO) hypoxia and hypoxic hypoxia vs. Baseline / pH compensation was evaluated on Pulmonary ventilation, CaO2, PaO2, pHa, blood pressure and heart rate. In unanaesthetized Bufo paracnemis, reductions in arterial PO2 stimulated ventilation, whereas carboxyhaemoglobinaemia per se failed to increase ventilation when pH was compensated.
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