Abstract
Based on observations in the intestine1.2 heart3,4 and kidney5, as well as the liver6, the concept of “reperfusion injury” has gained increasing attention in the transplant and organ preservation literature. This hypothesis proposes that there may be a separate distinct injury independent of the cellular injury which occurs during hypoxia or ischemia, associated with the resupply of blood (or oxygen) to previously ischemic (or hypoxic) mammalian tissue. Additionally, this reperfusion injury, under many circumstances, may be greater than the initial hypoxic insult. It has been postulated that the conversion of xanthine dehydrogenase (XDH) to the free radical producing enzyme, xanthine oxidase (XOD), during ischemia underlies this phenomenon. It is presumed that ATP breakdown7 during the period of ischemia leads to the accumulation of the XOD substrate hypoxanthine, although the co-substrate, oxygen, is in limited supply. During reperfusion, oxygen is re-introduced and a burst of free radical production and cell injury ensues8,9.
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Brass, C.A., Gollan, J.L. (1993). Biochemical Basis Of Hepatic Ischemic/Reperfusion Injury. In: Galmarini, D., Fassati, L.R., Paoletti, R., Sherlock, S. (eds) Drugs and the Liver: High Risk Patients and Transplantation. Medical Science Symposia Series, vol 4. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-1994-8_2
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DOI: https://doi.org/10.1007/978-94-011-1994-8_2
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