Hydrogen Gas Protects Transplant Livers from Cardiac Death Donors
- Authors
- 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
- Journal
- Surgery Today
- Year
- 2018
- DOI
- 10.1007/s00595-018-1693-0
- Study Type
- Rat
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Ischemia Reperfusion Injury
- Body System
- Hepatic
TL;DR
Hydrogen gas treatment significantly reduced damage to rat livers from lack of blood flow and oxygen after being stored and then reconnected to blood circulation.
Key Finding
Hydrogen gas treatment significantly reduced liver damage markers, preserved blood flow and energy production, and suppressed cell death pathways in rat livers subjected to ischemia reperfusion injury during simulated transplant conditions.
Summary
This study tested whether hydrogen gas could reduce damage to rat livers that had been deprived of oxygen (a condition called ischemia reperfusion injury) during organ transplant procedures. Researchers harvested livers from rats after cardiac arrest, stored them for 4 hours, then reperfused them with either normal oxygenated solution or solution containing hydrogen gas. Livers treated with hydrogen gas showed significantly less damage, better energy production, improved blood flow, and suppressed cell death pathways compared to untreated livers.
Practical Takeaway
This is a preliminary rat study showing hydrogen gas may help protect donor livers during transplantation, but it does not yet demonstrate effects in humans or through drinking hydrogen water. Much more research would be needed before any clinical applications could be considered.
Abstract
Background and purpose: We reported previously that hydrogen gas (H2) reduced hepatic ischemia and reperfusion injury (IRI) after prolonged cold storage (CS) of livers retrieved from heart-beating donors. The present study was designed to assess whether H2 reduced hepatic IRI during donation of a cardiac death (DCD) graft with subsequent CS. Methods: Rat livers were harvested after 30-min cardiac arrest and stored for 4 h in University of Wisconsin solution. 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. Results: 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. Conclusion: 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.