Effect of deferoxamine on late deaths following CPR in rats

Abstract

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.

Individual and synergistic antioxidative actions of melatonin: studies with vitamin E, vitamin C, glutathione and desferrrioxamine (desferoxamine) in rat liver homogenates

“…In-vivo it is known that the administration of ferrous salts exacerbates lipid peroxidation (Farber 1994). Also, chelation therapy in animals decreases lipid peroxidation and brain oedema and enhances survival (Komara et al 1986 ;Kompala et al 1986).…”