Oxygen-related chemoreceptor drive to breathe during H2S infusion

•Acute hyperoxic exposure does not reduce H2S-induced hyperpnea.•Acute hyperoxia does not decrease the level of dissolved H2S in the arterial blood during H2S infusion.•O2 is not sensed in the carotid body through rapid and reversible alteration in H2S rate of oxidation.

This study addresses the following question: Could the acute depression in breathing produced by hyperoxia, a reflection of the tonic drive to breathe from the arterial chemoreceptors, be accounted for by a background level of endogenous H2S? To address this question, we produced a stable but moderate increase in breathing (24 ± 11%) via continuous infusion of low levels of H2S, in 10 spontaneously breathing urethane-sedated rats. We found that acute exposure to 100% O2 (20 tests) decreased minute ventilation (V˙I) from 301 ± 51 to 210 ± 43 ml/min within 15 s in control conditions, but no additional significant drop in V˙I was observed during H2S induced hyperpnea. In addition, no decrease in the estimated concentrations of gaseous H2S in the arterial blood was observed during the hyperoxic tests. It is concluded that the ventilatory depression induced by high O2 appears to be limited to the tonic background peripheral chemosensory drive to breathe, but has little or no impact on the CB stimulation produced by low levels of H2S.