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Endothelial cell damage and Kupffer cell activation in reperfusion injury to livers stored for transplantation

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Procurement, Preservation and Allocation of Vascularized Organs

Abstract

Liver transplantation is an accepted therapy that achieves good long-term survival and a return to productive life for children and adults with end-stage liver disease. Scarcity of donor organs and graft dysfunction or failure are major obstacles to more widespread and successful application of liver transplantation surgery. In the USA alone, more than 2000 patients await donor livers, and hundreds die each year because none can be found [1]. In addition, primary non-function of grafts leading to graft failure and retransplantation occurs in 5–15% of patients [2–4]. Initial poor function of transplanted liver grafts occurs in another 20% of patients [5,6]. Since the clinical incidence of primary non-function is strongly dependent on time of cold storage, its aetiology is related to injury associated with graft harvest, storage and reperfusion. Liver damage after cold ischaemic storage is a special instance of the more general phenomenon of ischaemia/reperfusion injury. Recent advances in the understanding of storage/reperfusion injury reveal the many facets of this injury, virtually all of which are applicable to reperfusion injury after warm ischaemia to liver and other organs.

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Lemasters, J.J., Thurman, R.G. (1997). Endothelial cell damage and Kupffer cell activation in reperfusion injury to livers stored for transplantation. In: Collins, G.M., Dubernard, J.M., Land, W., Persijn, G.G. (eds) Procurement, Preservation and Allocation of Vascularized Organs. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-5422-2_15

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