Abstract
A number of mechanisms have been invoked to explain ischemia-induced tissue injury. One of these mechanisms, the production of oxygen-derived free radicals, has received particular attention in recent years. Oxygen-derived free radicals appear to play a major role in the pathogenesis of ischemia-reperfusion injury to digestive organs, such as the intestine,1,2,3,4 stomach,5 liver6 and pancreas.7 This assertion is largely based on observations that free radical scavengers significantly attenuate the microvascular and parenchymal damage associated with reperfusion of ischemic tissues. Also, when oxygen radicals are generated experimentally, the tissue damage produced mimics that observed after ischemia-reperfusion.8 Evidence to support the involvement of oxygen-derived free radicals in ischemic tissue injury also comes from studies of the coronary,9,10,11 renal12,13 and cutaneous circulations.14
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Hernandez, L.A., Grisham, M.B., Granger, D.N. (1987). Effects of Cu-Dips on Ischemia-Reperfusion Injury. In: Sorenson, J.R.J. (eds) Biology of Copper Complexes. Experimental Biology and Medicine, vol 16. Humana Press. https://doi.org/10.1007/978-1-4612-4584-1_16
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DOI: https://doi.org/10.1007/978-1-4612-4584-1_16
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