Inhibition of Hepatic Ischemic Reperfusion Injury Using Saline Exposed to Electron Discharge in a Rat Model.

Abstract

The pathogenesis of ischemia/reperfusion (I/R) injury in surgical trauma, organ transplantations, and brain and myocardial infarctions is attributable to excessive oxidative stress caused by reactive oxygen species and their metabolites. We prepared a physiological saline solution treated with simple exposure to a microampere current with electron discharge onto the surface; this treatment increased reduction potential and caused proton reduction. We examined the reductive potency of the electron-treated solution (ETS) on hepatocellular I/R injury in a rat model. When the ETS was administered in four doses at 0, 3, 10, and 20 min after reperfusion, severe hepatocellular injury was suppressed, as revealed by a decrease in serum alanine aminotransferase levels and histopathological improvement of liver damage. Since a preparation of hydrogen gas-dissolved saline solution (HDS) was shown to be capable of suppressing I/R injury, the possible involvement of dissolved hydrogen gas in the effectiveness of ETS was examined. When HDS was treated by degasification, the aforementioned effectiveness was decreased. In contrast, the same treatment did not alter the effectiveness of ETS. These results suggest that the antioxidative efficacy of ETS is not attributable to dissolved hydrogen gas but presumably to the molecule(s) produced from the stepwise reduction of protons in the solution.