Pathophysiology of ischemia-reperfusion injury and its management with hyperbaric oxygen (HBO): a review

Abstract

Here you will find the description of the pathophysiology of ischemia-reperfusion injury (IRI) and its treatment with hyperbaric oxygen therapy (HBOT). It includes a revision of peer-reviewed medical literature published in PubMed, regarding the pathophysiology of IRI and its management with hyperbaric oxygen (HBO). All the acute lesions, in the first 72 h, present a pathophysiology compatible with IRI. IRI has stages and involves ischemic and metabolic penumbras. Cellular hypoxia generates mitochondrial dysfunction, oxidative damage, activation of several inflammatory cascades, complement activation and eventually tissue death. HBOT restores oxygen tension maintaining cellular metabolism, restores ATP production, avoids or reduces mitochondrial dysfunction, prevents oxidative stress and apoptosis; and generates a secondary antioxidant production effect. All this, help to recover the marginal tissue, metabolic and ischemic penumbra, reduces cellular and tissue edema, promotes production of growth factors and enhances wound healing. The IRI requires a prompt response due to the short window of treatment. Adding HBOT to the early management could promote tissue survival by modifying ischemia, hypoxia, inflammation, immune response, and IRI injury. To determine the real use of HBOT in IRI; randomized and controlled studies are needed, within the window of treatment (<6 h).