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Science
01 January 2025

Hydrogen Gas Therapy Falls Short Against REBOA-Induced Stress

New study reveals hydrogen inhalation therapy ineffective for managing oxidative stress from severe hemorrhagic shock treatment.

A recent study published in Scientific Reports suggests hydrogen gas inhalation therapy is unlikely to effectively mitigate oxidative stress induced by resuscitative endovascular balloon occlusion of the aorta (REBOA) during treatment for severe hemorrhagic shock. With the growing need to address traumatic injuries effectively, researchers sought to explore alternative therapies to minimize oxidative injury.

Hemorrhagic shock is recognized as one of the leading preventable causes of trauma-related deaths, particularly among the young. REBOA is increasingly utilized as an intervention to manage severe hemorrhagic shock by temporarily occluding the abdominal aorta, but it can also induce oxidative stress through ischemia-reperfusion injury (IRI), significantly increasing the risk of multiple organ failure.

The animal model study involved ten healthy female swine, observing the effects of hydrogen gas inhalation during and after the REBOA procedure. Hydrogen inhalation was initiated simultaneously with the occlusion of the artery, aiming to gauge its presence amid potentially toxic oxidative conditions. Despite expectations, results indicated no substantial differences between swine receiving hydrogen therapy and those treated conventionally, as survival rates, lactate levels, and other biomarkers remained largely unchanged.

Specifically, the study found no significant change in survival rates between the control group and the hydrogen group, with survival lasting identical through the experimental period. Lactate levels, often used to gauge metabolic distress, showed only slight lower tendencies during the procedure for the hydrogen group but fell short of statistical significance.

The findings raise important questions about the role of hydrogen gas inhalation therapy as an adjunct treatment for oxidative stress tied to post-REBOA injury. Though there may be slight overall trends of improvement, the differences observed did not meet statistical thresholds, making it clear the therapy fails to offer sufficient mitigation for the post-REBOA oxidative challenges faced by patients.

“Hydrogen gas inhalation therapy exhibited no significant difference compared to the control group... 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,” the authors noted, emphasizing the limitations of their study and the need for additional efforts to explore protective therapies for IRI.

This study reinvigorates the scientific dialogue surrounding REBOA treatment efficiency and our current approaches to managing trauma-induced complications. Researchers observed widespread tissue damage linked to REBOA, including significant changes within intestinal structures, which add to the conversation on the integration of new therapies before or during REBOA procedures.

The conclusions of this study, alongside previous research, highlight the pressing need to identify effective therapeutic strategies amid the challenges posed by oxidative stress and the resulting IRI. Researchers noted, “These changes did not demonstrate significant differences...,” calling attention to the underlying variability inherent within therapeutic efficacy.

Despite the historical success of hydrogen gas inhalation observed in other clinical situations, the results from this porcine model suggest it may not be the panacea for oxidative stress linked to REBOA protocols. Continuous exploratory studies are necessary to refine clinical methodologies and offer substantial evidence for their implementation before being clinically adopted.

Future investigations will likely need to look beyond existing frameworks of hydrogen therapy, seeking alternative compounds or combinations aimed at enhancing patient outcomes following REBOA and mitigating systemic oxidative stress.