General Research
Model: rat
Hydrogen-rich solution attenuates cold ischemia-reperfusion injury in rat liver transplantation
Simplified Version Available
How Hydrogen-Rich Solutions Can Help Make Organ Transplants Safer
A recent study found that hydrogen-rich solutions can help reduce the damage caused by ischemia-reperfusion injury in liver transplants. This could make organ transplants safer and more effective. The study's findings have important implications for human transplants and could improve outcomes for people waiting for a liver transplant.
Read Simplified ArticleAbstract
Publish Year 2019 Country Japan Rank Positive Journal BMC Gastroenterology Primary Topic Liver Secondary TopicSurgery/Transplantation Model Rat Tertiary TopicTransplantation/Graft Injury Vehicle Solution (Dissolved) pH Neutral Application Immersion Comparison Complement
Background
Methods: We used a hydrogen-rich water bath to dissolve hydrogen into solution and graft tissues and performed isogenic and orthotopic LT in Lewis rats with University of Wisconsin (UW) solution. Blood and tissue samples were collected 6 h after the reperfusion. Hepatic enzymes in serum were measured. Pathological findings including the expressions of cytokines and heme oxygenase (HO)-1 in liver tissues were evaluated.
Methods
Results: The concentration of hydrogen inside the graft tissues increased depending on the storage time, plateauing after 1 h. Serum liver enzyme levels were significantly lower and the histology score of liver damage markedly attenuated in the group given grafts preserved in hydrogen-rich UW solution than in the control group. The hydrogen-rich UW solution group also showed less oxidative damage and hepatocyte apoptosis than the control group, and the expression of proinflammatory cytokines tended to be lower while the protein levels of HO-1 were significantly increased (n = 3-12 per group, P < 0.05). Conclusions: Storage of liver grafts in hydrogen-rich UW solution resulted in superior functional and morphologic protection against IRI via the up-regulation of HO-1 expression.