Hemorrhagic shock is a significant cause of trauma-related mortality. Resuscitative endovascular balloon occlusion of the aorta (REBOA) is a less-invasive aortic occlusion maneuver for severe hemorrhagic shock but potentially inducing oxidative stress injuries. In an animal model, this study investigated hydrogen gas inhalation therapy's potential to mitigate post-REBOA ischemia-reperfusion injuries (IRIs). Ten healthy female swine underwent REBOA placement after induced 40% hemorrhagic shock. They were observed during the IRI phase after a 60-minute Zone 1 occlusion for 180 minutes until euthanasia. 2% hydrogen gas inhalation was started simultaneously with REBOA inflation in the hydrogen group. We evaluated survival time, lactate, and 8-hydroxy-2'-deoxyguanosine (8-OHdG) biomarkers, gross findings, and pathological grades. One swine in the control group died at 90 min, and the remaining animals survived throughout the experiment. Survival analysis showed no significant differences between the two groups (control vs. hydrogen, 4/5 vs. 5/5; Log-rank, P = 0.317). Lactate levels during and after REBOA suggested a tendency towards lower levels in the hydrogen group (10.5 ± 4.2 vs. 7.6 ± 2.3 mmol/L, peak, T = 90). Serum 8-OHdG concentrations showed a lower trend in the hydrogen group (Range: 0.12-0.32 vs. 0.11-0.19 ng/mL). The villi of the ileum were destroyed during REBOA inflation and after reperfusion. Changes in the pathological grade of the ileum demonstrated no significant differences in both groups (2.8 ± 1.0 vs. 2.0 ± 1.0, proximal ileum, T = 240). Hydrogen gas inhalation therapy exhibited no significant difference compared to the control group in survival, lactate level, 8-OHdG, and intestinal mucosal injury following REBOA in a hemorrhagic shock model. Although it may slightly reduce mortality, biomarkers, and intestinal pathology, hydrogen gas inhalation therapy was not shown to have sufficient evidence to mitigate REBOA-IRI.
Keywords: Hydrogen; Ischemia-reperfusion injury; Oxidative stress; REBOA; Resuscitative endovascular occlusion of the aorta.
© 2024. The Author(s).