Hydrogen sulfide oxidation and the arterial chemoreflex: effect of methemoglobin.

Endogenous H(2)S has been proposed to transduce the effects of hypoxia in the carotid bodies (CB). To test this hypothesis, we created a sink for endogenously produced H(2)S by inducing ∼10% methemoglobinemia via the injection of 250 mg of sodium nitrite in spontaneously breathing anaesthetized sheep. Methemoglobinemia has been shown to catalyze the oxidation of large quantities of sulfide in the blood and tissues. We found that the presence of metHb completely abolished the ventilatory stimulation induced by 10 mg NaHS (i.v.), which in control conditions mimicked the effects of breathing 6-7 tidal volumes of nitrogen, confirming the dramatic increase in the oxidative power of the blood for sulfide. The ventilatory responses to hypoxia (10% O(2)), nitrogen and hyperoxia were in no way depressed by the metHb. Our results demonstrate that the ventilatory chemoreflex is not depressed in the presence of a high oxidative capacity for sulfide and challenge the view that H(2)S transduces the effects of hypoxia in the CB.