Post-reperfusion hydrogen gas treatment ameliorates ischemia reperfusion injury in rat livers from donors after cardiac death: a preliminary study.
Takahisa Ishikawa, Shingo Shimada, Moto Fukai, Taichi Kimura, Kouhei Umemoto, Kengo Shibata, Masato Fujiyoshi, Sunao Fujiyoshi, Takahiro Hayasaka, Norio Kawamura, Nozomi Kobayashi, Tsuyoshi Shimamura, Akinobu Taketomi · Surgery today · 2018
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Independent study record
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H2HUBB TAKEAWAY
In the NT group, liver enzyme leakage, apoptosis, necrosis, energy depletion, redox status, impaired microcirculation, and bile production were indicative of severe IRI, whereas in the H₂ group these impairments were significantly suppressed. These results are preclinical and suggest molecular hydrogen's therapeutic potential in the condition studied. Further human research is needed to establish clinical effectiveness.
What the Researchers Studied
The present study was designed to assess whether H₂ reduced hepatic IRI during donation of a cardiac death (DCD) graft with subsequent CS.
How Molecular Hydrogen Was Used
The graft was reperfused with oxygenated buffer, with or without H₂ (H₂ or NT groups, respectively), at 37° for 90 min on isolated perfused rat liver apparatus.
What the Researchers Found
In the NT group, liver enzyme leakage, apoptosis, necrosis, energy depletion, redox status, impaired microcirculation, and bile production were indicative of severe IRI, whereas in the H₂ group these impairments were significantly suppressed. The phosphorylation of cytoplasmic MKK4 and JNK were enhanced in the NT group and suppressed in the H₂ group. NFkB-p65 and c-Fos in the nucleus were unexpectedly unchanged by IRI regardless of H₂ treatment, indicating the absence of inflammation in this model.
H₂ Mechanisms / Biological Findings
The source material reviewed did not establish a specific molecular hydrogen mechanism for the reported findings.
Authors’ Conclusion
The authors concluded that H₂ was observed to ameliorate IRI in the DCD liver by maintaining microcirculation, mitochondrial functions, and redox status, as well as suppressing the cytoplasmic MKK4-JNK-mediated cellular death pathway.