The concept of “buying time in suspended animation” [49] has been discussed in the literature for more than a century. Originally induced by rapid external body cooling, any pharmacological measure allowing for a therapeutic, on demand induction of 'suspended animation' is of particular interest because of the undesired side effects of hypothermia per se. Therefore, the landmark paper demonstrating that inhaling H2S could induce a reversible, suspended animation-like hypometabolism [3], produced much excitement among researchers in the field of shock and critical illness. Numerous pre-clinical studies are currently available on H2S-related organ protection, but the effects on energy metabolism remain a matter of debate. In this context, the well-established toxic blockade of cytochrome c oxidase by H2S may assume particular importance. Most studies so far suggest that the beneficial effects of H2S are at least in part independent of an H2S-induced metabolic depression and, in particular, any decrease in core temperature. However, other data suggest that H2S-related hypo-metabolism may enhance the organ-protective properties. The mechanism behind H2S-induced hypometa-bolism is still not fully understood, and, moreover, the feasibility of H2S-induced suspended animation in larger animals has been questioned. Clearly, if possible at all, achieving a suspended animation-like status in larger animals and humans will be more difficult and require much more time because of the small surface area/mass ratio. Again the available data are equivocal, suggesting that at least hibernating isolated organs remains an option. Even in larger species, data on the effects of H2S on mitochondrial function and morphology suggest that its supplementation during circulatory shock provides protective reduction rather than toxic inhibition of cellular respiration. Finally, according to the currently available literature, neither inhalation of gaseous H2S nor injection of the soluble sulfide salts, NaSH or Na2S, is likely to become part of clinical practice because of damage to the airway mucosa and possibly toxic peak sulfide concentrations, respectively, but slow H2S-releasing molecules may enable these limitations to be overcome. Hence, there is “nothing rotten about hydrogen sulfide's medical promise” [50], and H2S clearly remains a “hot molecule” [51] in the field of research for a possible pharmacological induction of suspended animation-like hypometabolism.