On the basis of studies performed in mice that showed H2S inhalation decreasing dramatically the metabolic rate, H2S was proposed as a means of protecting vital organs from traumatic or ischemic episodes in humans. Hypoxia has in fact also long been shown to induce hypometabolism. However, this effect is observed solely in small-sized animals with high over(V, ̇)O2 k g- 1, and not in large mammals. Thus, extrapolating the hypometabolic effect of H2S to large mammals is questionable and could be potentially dangerous. We measured metabolism in conscious mice (24 g) exposed to H2S (60 ppm) at an ambient temperature of 23-24 °C. H2S caused a rapid and large (50%) drop in gas exchange rate, which occurred independently of the change in body temperature. The metabolic response occurred within less than 3 min. In contrast, sheep, sedated with ketamine and weighing 74 kg did not exhibit any decrease in metabolic rate during a similar challenge at an ambient temperature of 22 °C. While a part of H2S induced hypometabolism in the mice is related to the reduction in activity, we speculate that the difference between sheep and mice may rely on the nature and the characteristics of the relationship between basal metabolic rate and body weight thus on the different mechanisms controlling resting metabolic rate according to body mass. Therefore, the proposed use of H2S administration as a way of protecting vital organs should be reconsidered in view of the lack of hypometabolic effect in a large sedated mammal and of H2S established toxicity.
All Science Journal Classification (ASJC) codes
- General Neuroscience
- Pulmonary and Respiratory Medicine