The iron chelating agent deferoxamine was studied in an animal model as post-resuscitation therapy to prevent late deaths and brain damage following total circulatory arrest and resuscitation. Cardio-respiratory arrest was induced by injection of cold, 1% KC1 into the left ventricles of ketamine anesthetized rats pretreated with succinylcholine chloride, and by discontinuation of positive pressure ventilation. CPR was begun after six minutes, and animals with return of spontaneous circulation were entered into the study. Within five minutes after return of spontaneous circulation, treated animals received deferoxamine (50 mg/kg, IV). At ten days, 16 of 25 (64%) of treated animals had survived without neurologic deficit, compared to nine of 25 (36%) of controls (chi square = 3.92, P < .05). Chelation of intracellular iron by deferoxamine may have prevented free-radical-mediated reactions that led to late deaths in control animals.
animal model, cardiac arrest, reactive oxygen species, sudden death, ventricular fibrillation
Date of this Version
Babbs, Charles F.; Kompala, Sushil D.; and Blaho, Karl E., "Effect of Deferoxamine on Late Deaths Following CPR in Rats" (1986). Weldon School of Biomedical Engineering Faculty Publications. Paper 69.