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      Preservation solutions for attenuation of ischemia–reperfusion injury in vascularized composite allotransplantation

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          Abstract

          Vascularized composite allotransplantation represents the final level of the reconstructive ladder, offering treatment options for severe tissue loss and functional deficiencies. Vascularized composite allotransplantation is particularly susceptible to ischemia–reperfusion injury and requires preservation techniques when subjected to extended storage times prior to transplantation. While static cold storage functions to reduce ischemic damage and is widely employed in clinical settings, there exists no consensus on the ideal preservation solution for vascularized composite allotransplantation. This review aims to highlight current clinical and experimental advances in preservation solution development and their critical role in attenuating ischemia–reperfusion injury in the context of vascularized composite allotransplantation.

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          Cell biology of ischemia/reperfusion injury.

          Theodore Kalogeris, Christopher P. Baines, Maike Krenz … (2012)
          Disorders characterized by ischemia/reperfusion (I/R), such as myocardial infarction, stroke, and peripheral vascular disease, continue to be among the most frequent causes of debilitating disease and death. Tissue injury and/or death occur as a result of the initial ischemic insult, which is determined primarily by the magnitude and duration of the interruption in the blood supply, and then subsequent damage induced by reperfusion. During prolonged ischemia, ATP levels and intracellular pH decrease as a result of anaerobic metabolism and lactate accumulation. As a consequence, ATPase-dependent ion transport mechanisms become dysfunctional, contributing to increased intracellular and mitochondrial calcium levels (calcium overload), cell swelling and rupture, and cell death by necrotic, necroptotic, apoptotic, and autophagic mechanisms. Although oxygen levels are restored upon reperfusion, a surge in the generation of reactive oxygen species occurs and proinflammatory neutrophils infiltrate ischemic tissues to exacerbate ischemic injury. The pathologic events induced by I/R orchestrate the opening of the mitochondrial permeability transition pore, which appears to represent a common end-effector of the pathologic events initiated by I/R. The aim of this treatise is to provide a comprehensive review of the mechanisms underlying the development of I/R injury, from which it should be apparent that a combination of molecular and cellular approaches targeting multiple pathologic processes to limit the extent of I/R injury must be adopted to enhance resistance to cell death and increase regenerative capacity in order to effect long-lasting repair of ischemic tissues. Copyright © 2012 Elsevier Inc. All rights reserved.
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            Reperfusion injury and reactive oxygen species: The evolution of a concept☆

            D. Granger, Peter R. Kvietys (2015)
            Reperfusion injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following the restoration of blood flow and tissue oxygenation, has been a focus of basic and clinical research for over 4-decades. While a variety of molecular mechanisms have been proposed to explain this phenomenon, excess production of reactive oxygen species (ROS) continues to receive much attention as a critical factor in the genesis of reperfusion injury. As a consequence, considerable effort has been devoted to identifying the dominant cellular and enzymatic sources of excess ROS production following ischemia-reperfusion (I/R). Of the potential ROS sources described to date, xanthine oxidase, NADPH oxidase (Nox), mitochondria, and uncoupled nitric oxide synthase have gained a status as the most likely contributors to reperfusion-induced oxidative stress and represent priority targets for therapeutic intervention against reperfusion-induced organ dysfunction and tissue damage. Although all four enzymatic sources are present in most tissues and are likely to play some role in reperfusion injury, priority and emphasis has been given to specific ROS sources that are enriched in certain tissues, such as xanthine oxidase in the gastrointestinal tract and mitochondria in the metabolically active heart and brain. The possibility that multiple ROS sources contribute to reperfusion injury in most tissues is supported by evidence demonstrating that redox-signaling enables ROS produced by one enzymatic source (e.g., Nox) to activate and enhance ROS production by a second source (e.g., mitochondria). This review provides a synopsis of the evidence implicating ROS in reperfusion injury, the clinical implications of this phenomenon, and summarizes current understanding of the four most frequently invoked enzymatic sources of ROS production in post-ischemic tissue.
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              Toxicity of iron and hydrogen peroxide: the Fenton reaction

              Christine Winterbourn (1995)
              Iron and hydrogen peroxide are capable of oxidizing a wide range of substrates and causing biological damage. The reaction, referred to as the Fenton reaction, is complex and capable of generating both hydroxyl radicals and higher oxidation states of the iron. The mechanism and how it is affected by different chelators, and the interpretation of results obtained in biological systems, are discussed.
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                Author and article information

                Journal
                Journal ID (nlm-ta): SAGE Open Med
                Journal ID (iso-abbrev): SAGE Open Med
                Journal ID (publisher-id): SMO
                Journal ID (hwp): spsmo
                Title: SAGE Open Medicine
                Publisher: SAGE Publications (Sage UK: London, England )
                ISSN (Electronic): 2050-3121
                Publication date (Electronic): 21 July 2021
                Publication date Collection: 2021
                Volume: 9
                Electronic Location Identifier: 20503121211034924
                Affiliations
                [1 ]Temerty Faculty of Medicine, University of Toronto, Toronto, ON, Canada
                [2 ]Latner Thoracic Surgery Laboratories, University Health Network, Toronto General Hospital, University of Toronto, Toronto, ON, Canada
                [3 ]Division of Plastic & Reconstructive Surgery, Department of Surgery, University of Toronto, Toronto, ON, Canada
                Author notes
                [*]Siba Haykal, Temerty Faculty of Medicine, University of Toronto, 200 Elizabeth Street 8N-869, Toronto, ON M5G 2C4, Canada. Email: Siba.haykal@ 123456uhn.ca
                Author information
                https://orcid.org/0000-0002-0855-3764
                https://orcid.org/0000-0002-4247-2810
                Article
                Publisher ID: 10.1177_20503121211034924
                DOI: 10.1177/20503121211034924
                PMC ID: 8312154
                PubMed ID: 34367640
                SO-VID: ec3a1f98-4f61-441d-99df-522629e52ce8
                Copyright © © The Author(s) 2021
                License:

                This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License ( https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages ( https://us.sagepub.com/en-us/nam/open-access-at-sage).

                History
                Date received : 8 July 2021
                Date accepted : 7 July 2021
                Categories
                Subject: Original Research Article
                Custom metadata
                cover-date January-December 2021
                typesetter ts1

                Keywords: vascularized composite allotransplantation,ischemia–reperfusion injury,preservation solution
                Data availability:
                Keywords: vascularized composite allotransplantation, ischemia–reperfusion injury, preservation solution

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