Brain iron delocalization and lipid peroxidation following cardiac arrest

Brain injury after cardiac arrest and resuscitation may occur, in part, by oxygen radical mechanisms. The availability of a transition metal, such as iron, is essential for in vitro initiation of this type of reaction. The brain has significant stores of iron bound in large proteins. We conducted this study to determine whether iron availability is enhanced in the canine brain following resuscitation from 15 minutes of cardiac arrest, and whether this iron is associated with the appearance of products of radical-mediated lipid peroxidation (LP) after two hours of reperfusion. Examination of the data by the method of multivariate analysis revealed significant increases in the low molecular weight species (LMWS) iron (300% of nonischemic controls, P less than .01), malondialdehyde (MDA), a lipid peroxidation degradation product (145% of nonischemic controls, P less than .01), and conjugated dienes (CD) (204% of nonischemic controls, P = .07). Therapy with deferoxamine (50 mg/kg IV immediately post resuscitation) produced a reduction in MDA and CD to levels statistically indistinguishable from nonischemic controls. We conclude that brain tissue iron is delocalized from normal storage forms to a LMWS pool after two hours of reperfusion following resuscitation from a 15-minute cardiac arrest, and that this is associated with increased products of LP. The increase in LP products is blocked by treatment with deferoxamine.