心臓手術後の腎障害に対する分子状水素の保護効果：豚モデルを用いた検討
Cardiac surgery-associated acute kidney injury is a frequent postoperative complication driven largely by elevated oxidative stress. Using a porcine model that simulated heart transplantation with 3 hours of extracorporeal circulation (ECC) followed by 60 minutes of spontaneous cardiac reperfusion, researchers assessed whether inhaled 4% H2 gas—administered during anesthesia and throughout ECC blood oxygenation—could protect renal function. Plasma concentrations of creatinine, urea, and phosphorus rose markedly in untreated surgical animals, whereas all three biomarkers returned to near-control levels in the hydrogen-treated group. Western blot analysis of renal tissue revealed activation of the Nrf2/Keap1 signaling pathway and upregulation of superoxide dismutase 1 (SOD1) protein in hydrogen-exposed animals. These findings indicate that H2 inhalation confers renoprotection in the context of cardiac surgery, likely through antioxidant pathway activation.
Inhaled H2 activates the Nrf2/Keap1 antioxidant signaling pathway and upregulates superoxide dismutase 1 (SOD1) protein expression in renal tissue, thereby reducing oxidative stress-mediated kidney damage following cardiac surgery with extracorporeal circulation.
For inhalation applications of molecular hydrogen, the lower flammability limit (LFL) deserves careful handling. The classical 4% figure applies to closed-system mixtures; the practical inhalation-environment threshold is 10%. Even pure-hydrogen output (the UFL 75% paradox) passes through the flammable range at the air–gas boundary. High-concentration (66% / 100%) inhalers are documented in the Japanese Consumer Affairs Agency accident-information database and are not recommended.
See also:
https://h2-papers.org/en/papers/37463517