Deferoxamine pretreatment reduces canine infarct size and oxidative injury

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Abstract

To test whether iron-catalyzed processes contribute to myocardial necrosis during ischemia and reperfusion, we administered the iron chelator, deferoxamine, to chloralose-anesthetized dogs subjected to 0 min of left anterior descending artery occlusion followed by 360 min of reperfusion. Deferoxamine blocks iron-catalyzed hydroxyl radical formation in vitro. Groups of dogs received either pretreatment with deferoxamine or iron-loaded deferoxamine (15 mg/kg over 30 min preocclusion and 2.5 mg/kg/hr during the first 120 min of reperfusion), equal volumes of saline or deferoxamine treatment during reperfusion (15 mg/kg over 30 min beginning at 75 min of occlusion followed by 2.5 mg/kg/hr during the remainder of the first 120 min of reperfusion). Infarct size as a percentage of area at risk was reduced (P

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Lesnefsky, E. J., Repine, J. E., & Horwitz, L. D. (1990). Deferoxamine pretreatment reduces canine infarct size and oxidative injury. Journal of Pharmacology and Experimental Therapeutics, 253(3), 1103–1109. https://doi.org/10.1016/s0022-3565(25)13209-6

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