1.2% Hydrogen gas inhalation protects the endothelial glycocalyx during hemorrhagic shock: a prospective laboratory study in rats

Purpose: Hydrogen gas (H₂) inhalation improved the survival rate of hemorrhagic shock. However, its mechanisms are unknown. We hypothesized that H₂ protected the endothelial glycocalyx during hemorrhagic shock and prolonged survival time. Methods: 83 Sprague–Dawley rats were anesthetized with isoflurane. The animals were randomly assigned to 5 groups: room air with no shock, 1.2% H₂ with no shock, room air with shock (Control-S), 1.2% H₂ with shock (H₂1.2%-S), and 3.0% H₂ with shock (H₂3.0%-S). Shock groups were bled to a mean arterial pressure of 30–35 mmHg and held for 60 min, then resuscitated with normal saline at fourfold the amount of the shed blood volume. Results: The syndecan-1 level was significantly lower in the H₂1.2%-S [8.3 ± 6.6 ng/ml; P = 0.01; 95% confidence interval (CI), 3.2–35.8] than in the Control-S (27.9 ± 17.0 ng/ml). The endothelial glycocalyx was significantly thicker in the H₂1.2%-S (0.15 ± 0.02 µm; P = 0.007; 95% CI, 0.02–0.2) than in the Control-S (0.06 ± 0.02 µm). The survival time was longer in the H₂1.2%-S (327 ± 67 min, P = 0.0160) than in the Control-S (246 ± 69 min). The hemoglobin level was significantly lower in the H₂1.2%-S (9.4 ± 0.5 g/dl; P = 0.0034; 95% CI, 0.6–2.9) than in the Control-S (11.1 ± 0.8 g/dl). However, the H₂3.0%-S was not significant. Conclusions: Inhalation of 1.2% H₂ gas protected the endothelial glycocalyx and prolonged survival time during hemorrhagic shock. Therapeutic efficacy might vary depending on the concentration.