LPS誘発全身性炎症モデルにおける分子状水素の体温調節・心血管・炎症パラメータへの影響
Male Wistar rats (250–300 g) received intravenous LPS at 0.1 or 1.5 mg/kg to induce mild or severe systemic inflammation, followed by 360-minute inhalation of 2% H₂ gas. Deep body temperature was monitored via intraperitoneally implanted dataloggers. Under mild inflammation, H₂ inhalation suppressed plasma TNF-α and IL-6 surges, elevated the anti-inflammatory cytokine IL-10, and prevented fever. Under severe inflammation, H₂ potentiated hypothermia and prevented both fever and hypotension; these outcomes coincided with reduced plasma nitric oxide production, decreased TNF-α and IL-1β levels, and lower prostaglandin E₂ (PGE₂) concentrations in both plasma and hypothalamus. H₂ had no measurable effect on cardiovascular, inflammatory, or thermoregulatory parameters in saline-treated control animals. The findings indicate that H₂ modulates febrile and hemodynamic responses in systemic inflammation through suppression of pro-inflammatory mediators and hypothalamic PGE₂ signaling.
H₂ inhalation reduces plasma nitric oxide production and suppresses pro-inflammatory mediators (TNF-α, IL-1β, PGE₂) while elevating IL-10, thereby downregulating hypothalamic febrile signaling and attenuating thermoregulatory and hemodynamic dysregulation during systemic inflammation.
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.
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https://h2-papers.org/en/papers/30261305