Abstract
A critical factor in the extreme shortage of livers for transplantation is frequent failure due to primary non-function of ethanol-induced fatty livers when employed as donor organs (Starzl et all., 1988). Although fatty livers due to ethanol are frequently available in the donor pool since a major source of liver grafts is brain-dead victims of accidents involving alcohol (Butts & Patetta, 1988), surgeons must sometimes discard these organs because of high lipid content. Thus, an examination of the relationship between alcohol, fatty liver, and graft failure following liver transplantation could lead to a larger donor pool of usable organs. With this as a goal, we examined the connection between Kupffer cells and reperfusion injury in ethanol-induced fatty liver since Kupffer cells, which are activated following cold storage and reperfusion (Thurman, Cowper, Marzi, Currin, & Lemasters, 1988), have been implicated in primary non-function. Kupffer cells, when activated, release toxic mediators including cytokines and eicosanoids (Decker, 1990) which may play a role in reperfusion injury following transplantation.
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Thurman, R.G. et al. (1996). Role of Free Radicals in Failure of Fatty Livers following Liver Transplantation and Alcoholic Liver Injury. In: Snyder, R., et al. Biological Reactive Intermediates V. Advances in Experimental Medicine and Biology, vol 387. Springer, Boston, MA. https://doi.org/10.1007/978-1-4757-9480-9_31
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DOI: https://doi.org/10.1007/978-1-4757-9480-9_31
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