• Y Sleiman, S Hafner, M Groeger, S Weber, P Radermacher, and E Calzia.
• Department of Anesthesiological Pathophysiology and Process Development, Ulm, Germany.
• Shock. 2015 Oct 1;44 Suppl 2:24.

IntroductionEndogenous hydrogen sulfide (H2S) has been recently recognized as a molecule fundamentally involved in the regulation of mitochondrial bioenergetics. Therefore we aimed to compare maximum mitochondrial respiratory activity (JO2max) as well as the degree of coupling (L/E-ratio) in small homogenized liver and kidney tissue biopsies from wildtype (WT) and cystathionine γ-lyase (CSE)-KO mice who underwent an experimental thoracic trauma (TXT) or not (Sham).MethodsAnesthetized and mechanically ventilated mice were observed for 4 hours after a standardized thoracic trauma; Sham animals were treated in the same way except of the experimental trauma. At the end of the observation period the biopsies were sampled, homogenized, and used for quantifying mitochondrial respiration by means of the high-resolution respirometry in an O2K-Oxygraph (Oroboros® Inst., Austria). JO2max was achieved by adding 5 mM malate, 10 mM glutamate, 10 mM pyruvate, 10 mM succinate as substrates together with 5 mM ADP. L/E was determined after further addition of 5 μM oligomycine and 1 μM of the protonophore FCCP.ResultsJO2max remains almost stable in CSE-deficient animals. However, the degree of coupling was slightly increased in this group, albeit these effect was statistically significant in the liver tissue of the TxT-group only. In contrast to CSE-KO, TxT alone poorly affected mitochondrial respiration.ConclusionWe conclude that after a standardized thoracic trauma CSE deficiency only slightly influences mitochondrial respiration. The changes in the L/E-ratio probably result from compensatory mechanisms.

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