Rewarming Injury after Cold Preservation
AbstractOrgan dysfunction pertinent to tissue injury related to ischemic ex vivo preservation during transport from donor to recipient still represents a pivotal impediment in transplantation medicine. Cold storage under anoxic conditions minimizes metabolic activity, but eventually cannot prevent energetic depletion and impairment of cellular signal homeostasis. Reoxygenation of anoxically injured tissue may trigger additional damage to the graft, e.g., by abundant production of oxygen free radicals upon abrupt reactivation of a not yet equilibrated cellular metabolism. Paradoxically, this process is driven by the sudden restoration of normothermic conditions upon reperfusion and substantially less pronounced during re-oxygenation in the cold. The massive energy demand associated with normothermia is not met by the cellular systems that still suffer from hypothermic torpor and dys-equilibrated metabolites and eventually leads to mitochondrial damage, induction of apoptosis and inflammatory responses. This rewarming injury is partly alleviated by preceding supply of oxygen already in the cold but more effectively counteracted by an ensuing controlled and slow oxygenated warming up of the organ prior to implantation. A gentle restitution of metabolic turnover rates in line with the resumption of enzyme kinetics and molecular homeostasis improves post transplantation graft function and survival. View Full-Text
Share & Cite This Article
Minor, T.; von Horn, C. Rewarming Injury after Cold Preservation. Int. J. Mol. Sci. 2019, 20, 2059.
Minor T, von Horn C. Rewarming Injury after Cold Preservation. International Journal of Molecular Sciences. 2019; 20(9):2059.Chicago/Turabian Style
Minor, Thomas; von Horn, Charlotte. 2019. "Rewarming Injury after Cold Preservation." Int. J. Mol. Sci. 20, no. 9: 2059.
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.