亜硝酸水銀誘発性急性腎障害の多尿期におけるno-reflow症候群に対する分子状水素の効果
Using a rat model of sublimate nephropathy (mercuric chloride 5 mg/kg subcutaneously, hyposodium diet, 72-hour observation), this study examined whether hydrogen-rich water loading (1.2 ppm H2, redox potential −100 to −350 mV) could correct no-reflow syndrome during the early polyuric stage of acute kidney injury. Sixty male rats were divided into experimental groups. Hydrogen-rich water administration was associated with reduced lipid peroxidation in the renal cortex, improved sodium and β2-microglobulin reabsorption in the proximal tubule, an elevated K⁺/Na⁺ ratio, and diminished renal edema across seven tissue layers. Total and enzymatic fibrinolytic activity in the renal cortex increased, and succinate dehydrogenase activity rose, attributed to enhanced electron delivery via the negative redox potential. The findings suggest that selective neutralization of hydroxyl radicals and peroxynitrite by molecular hydrogen can interrupt both large and small pathological feedback loops underlying no-reflow syndrome in this model.
Molecular hydrogen selectively scavenges hydroxyl radicals and peroxynitrite, reducing lipid peroxidation in the renal cortex, thereby restoring proximal tubular reabsorption and enhancing fibrinolytic activity while its negative redox potential supports mitochondrial electron transport via succinate dehydrogenase.
Hydrogen-rich water is a low-risk delivery route, but the achievable systemic hydrogen dose is bounded. For clinical applications, inhalation is the most efficient route; inhalation, however, carries explosion risk, and concentration matters (empirical LFL of 10% applies to inhalation environments; high-concentration devices are documented in the Consumer Affairs Agency accident database and are not recommended).
See also:
https://h2-papers.org/en/papers/33814411