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Open Badges Commentary

Endogenous H2S in hemorrhagic shock: innocent bystander or central player?

Enrico Calzia1*, Peter Radermacher1 and Kenneth R Olson2

Author Affiliations

1 Sektion Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Klinik für Anästhesiologie, Universitätsklinikum Ulm, Helmholtzstrasse 8-1, D-89081 Ulm, Germany

2 Department of Physiology, Indiana University School of Medicine, 1234 Notre Dame Avenue, South Bend, IN 46617, USA

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Critical Care 2012, 16:183  doi:10.1186/cc11833

See related research by Van de Louw and Haouzi, and related letter by Haouzi,

Published: 29 November 2012


The role of the gaseous mediator hydrogen sulfide (H2S) in hemorrhagic shock is still a matter of debate. This debate is emphasized by the fact that available literature data on blood and tissue H2S concentrations vary by three orders of magnitude, both under physiological conditions as well as during stress states. Therefore, in a rat model of unresuscitated, lethal hemorrhagic shock, Van de Louw and Haouzi tested the two hypotheses of whether blood and tissue H2S levels would increase due to the shock-related tissue hypoxia, and whether vitamin B12 would attenuate organ injury and improve survival as a result of enhanced H2S oxidation. Hemorrhage did not affect the blood and tissue H2S content, and, despite the increased capacity to oxidize H2S, vitamin B12 did not affect any parameter of shock severity. The authors concluded that H2S concentrations cannot be used as a marker of shock, most probably as a result of tissue's capacity to oxidize H2S even under conditions of severe oxygen debt. This research paper elegantly re-adjusts the currently available data on blood and tissue H2S levels, and thereby adds an important piece to the puzzle of whether H2S release should be enhanced or lowered during stress conditions associated with tissue hypoxia.