Hypoxia alters the control of breathing and metabolism by increasing ventilation through the arterial chemoreflex, an effect which, in small-sized animals, is offset by a centrally mediated reduction in metabolism and respiration. We tested the hypothesis that hydrogen sulfide (H2S) is involved in transducing these effects in mammals. The rationale for this hypothesis is twofold. Firstly, inhalation of a 20-80 ppm H2S reduces metabolism in small mammals and this effect is analogous to that of hypoxia. Secondly, endogenous H2S appears to mediate some of the cardio-vascular effects of hypoxia in non-mammalian species. We, therefore, compared the ventilatory and metabolic effects of exposure to 60 ppm H2S and to 10% O2 in small and large rodents (20 g mice and 700 g rats) wherein the metabolic response to hypoxia has been shown to differ according to body mass. H2S and hypoxia produced profound depression in metabolic rate in the mice, but not in the large rats. The depression was much faster with H2S than with hypoxia. The relative hyperventilation produced by hypoxia in the mice was replaced by a depression with H2S, which paralleled the drop in metabolic rate. In the larger rats, ventilation was stimulated in hypoxia, with no change in metabolism, while H2S affected neither breathing nor metabolism. When mice were simultaneously exposed to H2S and hypoxia, the stimulatory effects of hypoxia on breathing were abolished, and a much larger respiratory and metabolic depression was observed than with H2S alone. H2S had, therefore, no stimulatory effect on the arterial chemoreflex. The ventilatory depression during hypoxia and H2S in small mammals appears to be dependent upon the ability to decrease metabolism.
- Arterial chemoreception
- Oxygen transduction