Is Pharmacological, H2S-induced ‘Suspended Animation’ Feasible in the ICU?

Asfar, Pierre; Calzia, Enrico; Radermacher, Peter

doi:10.1007/978-3-319-03746-2_58

Cited by 1 publication

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References 51 publications

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“…Inhaling gaseous H 2 S or injection of the soluble sulfide salts NaSH or Na 2 S most likely will not become clinical practice due to damage of airway mucosa and possibly toxic peak sulfide concentrations, but slow H 2 S-releasing molecules may allow avoiding these problems. Despite the promising findings in rodent models [1–3,16,49,50], the role of a possible H 2 S-induced hypometabolism during shock states is unclear as well [123]: most studies so far suggest that any beneficial effect of H 2 S is at least in part independent of metabolic depression, but other data suggest that H 2 S-related hypometabolism may enhance its organ-protective properties. In addition, while the feasibility per se of on demand, H 2 S-induced protective reduction rather than toxic inhibition of cellular respiration is still matter of debate, “hibernating” isolated organs remains an option.…”

Section: Introductionmentioning

confidence: 99%

H2S during circulatory shock: Some unresolved questions

et al. 2014

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Numerous papers have been published on the role of H2S during circulatory shock. Consequently, knowledge about vascular sulfide concentrations may assume major importance, in particular in the context of “acute on chronic disease”, i.e., during circulatory shock in animals with pre-existing chronic disease. This review addresses the questions i) of the “real” sulfide levels during circulatory shock, and, ii) to which extent injury and pre-existing co-morbidity may affect the expression of H2S producing enzymes under these conditions. In the literature there is a huge range on sulfide blood levels during circulatory shock, in part as a result of the different analytical methods used, but also due to the variable of the models and species studied. Clearly, some of the very high levels reported should be questioned in the context of the well-known H2S toxicity. As long as “real” sulfide levels during circulatory shock are unknown and/or undetectable “on line” due to the lack of appropriate techniques, it appears to be premature to correlate the measured blood levels of hydrogen sulfide with the severity of shock or the H2S therapy-related biological outcomes. The available data on the tissue expression of the H2S-releasing enzymes during circulatory shock suggest that a “constitutive” CSE expression may play a crucial role of for the maintenance of organ function, at least in the kidney. The data also indicate that increased CBS and CSE expression, in particular in the lung and the liver, represents an adaptive response to stress states.

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