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Hydrogen gas has emerged as a therapeutic tool for various entities involving ischemia–reperfusion injury (IRI). Animal studies have shown that inhaled hydrogen gas protects against spinal cord IRI. Kimura and colleagues
take another step forward, revealing a potential mechanism for these beneficial effects.
In their comprehensive, well-designed, prospective, randomized rat study, they reveal that inhalation of varying levels of hydrogen gas (1%, 2%, or 3%) before standard induction of spinal cord IRI exerts concentration-dependent protective effects on motor function, seen via histopathologic examination. Furthermore, inhaled hydrogen gas also attenuated spinal cord IRI-induced increases in ventral horn glutamate levels in a concentration-dependent manner. Lastly, the protective effects of inhaled hydrogen gas were not observed in animals receiving a glutamate transporter-1 inhibitor and ventral horn glutamate levels increased in these animals as well. Their results confirm findings of other investigators demonstrating spinal cord IRI-protective effects of inhaled hydrogen gas. Their results also indicate that glutamate transporter-1 may play an important role in this process.
Despite advances in surgical techniques, spinal cord IRI remains a significant problem after both open repair and endovascular thoracoabdominal aneurysm repair, with incidence reported from 10% to 30%.
Mechanism of spinal cord IRI is postulated to be caused by alterations in spinal cord perfusion pressure; due to hypotension, increased cerebrospinal fluid (CSF) pressure, or interruption of flow through segmental arteries (SAs) during aortic clamping or during reperfusion after unclamping.
Cause of spinal cord IRI during endovascular thoracoabdominal aneurysm repair is believed to be due to coverage of SAs by graft location, yet a recent pilot study shows magnetic resonance imaging and histologic findings of spinal cord IRI in endovascular thoracoabdominal aneurysm repair may be much different then open repair, suggesting a different mechanism of injury.
Goals of management strategies address these disparate causes. CSF drainage, among the most studied options, involves perioperative intrathecal catheter placement, with goal of decreasing CSF pressure.
Other options include selective reimplantation of SAs or distal aortic perfusion via an atriofemoral bypass circuit. Pharmacologic interventions such as corticosteroids or barbiturates act to decrease metabolic rate of the spinal cord or function as free radical scavengers to minimize reperfusion injury.
Despite the vast number of various strategies available, no single tactic has proven sufficient to completely abolish spinal cord IRI. Hydrogen gas may be effective in reducing oxidative stress after cardiac arrest, and is now potentially effective against spinal cord IRI.
The ability to potentially have a universal, safe, and easily applied technique to avoid the devastating results of spinal cord IRI is a very exciting prospect, and the results of this study conducted by Kimura and colleagues
Disclosures: The authors reported no conflicts of interest.
The Journal policy requires editors and reviewers to disclose conflicts of interest and to decline handling or reviewing manuscripts for which they may have a conflict of interest. The editors and reviewers of this article have no conflicts of interest.
This experimental study aimed to assess the efficacy of hydrogen gas inhalation against spinal cord ischemia–reperfusion injury and reveal its mechanism by measuring glutamate concentration in the ventral horn using an in vivo microdialysis method.
Treating acute myocardial infarction should not be like shooting flies with a cannon; the target is the ischemic heart only, and a specifically targeted local treatment decreases risks of systematic side effects. The key is to bring the treatment to the specific tissue area intended to heal without influencing unnecessarily the whole of the body.