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Title: The iron chelator desferrioxamine attenuates postischemic ventricular dysfunction

Journal Article · · American Journal of Physiology; (USA)
OSTI ID:6945534

Recent evidence suggests that postischemic myocardial dysfunction (stunning) may be mediated by oxygen free radicals, but the mechanism by which they produce myocellular damage remains unknown. Since iron catalyzes formation of hydroxyl radicals (HO{center dot}) as well as HO{center dot}-initiated lipid peroxidation, the authors explored the potential role of this metal in the pathogenesis of myocardial stunning. Open-chest dogs undergoing a 15-min occlusion of the left anterior descending coronary artery (LAD) followed by 4 h of reperfusion (REP) received the iron chelator desferrioxamine intravenously or normal saline. Regional myocardial function was assessed by measuring systolic wall thickening with an epicardial Doppler probe. The two groups exhibited comparable systolic thickening under base-line conditions and similar degrees of dyskinesis during ischemia. After REP, however, recovery of contractile function as considerably greater in desferrioxamine-treated compared with control dogs. These differences could not be ascribed to hemodynamic factors. The results suggest that iron-catalyzed reactions (possibly HO{center dot} generation) play a significant role in myocardial stunning after a brief episode of reversible regional ischemia.

OSTI ID:
6945534
Journal Information:
American Journal of Physiology; (USA), Vol. 253:6; ISSN 0002-9513
Country of Publication:
United States
Language:
English