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Acta Physiologica Congress

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Acta Physiologica 2011; Volume 202, Supplement 684
The Joint Conference (FAMÉ 2011) of the LXXVth Meeting of the Hungarian Physiological Society, XVIth Meeting of the Hungarian Society of Anatomists, Experimental Section of the Hungarian Society for Experimental and Clinical Pharmacology and Hungarian Society for Microcirculation and Vascular Biology
6/8/2011-6/11/2011
Pécs, Hungary


H2S FROM ROTTEN EGG TO SUSPENDED ANIMATION
Abstract number: L7

Hauser1 B., Radermacher2 P., Gal1 J.

Aims: 

Hydrogen sulfide (H2S) is a toxic gas which deserved attention as the third gaseous transmitter, a signaling molecule regulating important biological processes. The aim of this presentation is to review some of the recent data about experimental therapeutic application of H2S on rodent as well as on large animal models of shock, sepsis and ischemia reperfusion.

Methods and results: 

Endogenous or exogenous H2S has multiple actions, including inhibition of mitochondrial respiration, cytoprotective, vasodilatory, antioxidant and antiapoptotic effects, induction of suspended animation, and a friend or foe character as a potential inflammatory mediator (Baumgart 2009). It is applicable via inhalation or as an intravenous infusion (H2S donor Na2S), and has a half-life of minutes within the body. In a landmark paper (Blackstone 2005) mice exposed to H2S inhalation reached a reversible hibernation-like state (suspended animation) with decreased energy expenditure and decreased body temperature. In anesthetized and ventilated mice inhaled H2S offered metabolic benefit during therapeutic hypothermia in terms of improved yield of mitochondrial respiration (Baumgart 2010). During resuscitated murine sepsis the anti-inflammatory effects of inhaled H2S has been attenuated by sepsis (Wagner 2011). In a porcine model of aortic occlusion induced ischemia/reperfusion injury intravenous H2S reduced energy expenditure and improved noradrenaline responsiveness during reperfusion but parameters of oxidative stress or inflammation were not affected (Simon 2008). On virtually the same model but using longer ischemic period (90min vs. 30min) intravenous H2S ameliorated organ dysfunction and glomerular histological damage and attenuated oxidative stress, NO production and systemic inflammation (Simon 2011). In hemorrhagic shock in rats H2S has been found pro-inflammatory (Mok 2008) and in pigs in one model H2S improved survival (Bracht 2010) while it failed to do so in another one (Drabek 2011).

Conclusion: 

Based on preclinical data H2S has a possible therapeutic potential on organ protection (Szabó 2007) in different models, however, further investigations are warranted.

To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 202, Supplement 684 :L7

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