Post resuscitation iron delocalization and malondialdehyde production in the brain following prolonged cardiac arrest.

Assays for brain tissue malondialdehyde (MDA) and low molecular weight chelated (LMWC) iron were used to examine samples of the cerebral cortex obtained from dogs 2 h after resuscitation from a 15-min cardiac arrest. The effect of post-resuscitation treatment with lidoflazine and/or desferrioxamine was similarly examined. Non-ischemic brain samples had LMWC iron levels (in nmol/100 mg tissue) of 12.32 + 2.60 and MDA levels (in nmol/100 mg tissue) of 8.46 + 1.35. Animals subjected to cardiac arrest and resuscitation and standard intensive care (SIC) had LMWC iron levels of 37.04 + 4.58 (p less than .01 against non-ischemic controls) and MDA levels of 12.24 + 1.9 (p less than .05 against non-ischemic controls). All treatment interventions significantly reduced the LMWC iron (p less than .05), but only treatment with desferrioxamine alone significantly reduced MDA (p less than .05), although a trend toward reduction of the MDA was also evident in animals treated with both desferrioxamine and lidoflazine. LMWC iron levels are increased in the post-ischemic brain, and this increase may be related to lipid peroxidation in the brain following resuscitation from cardiac arrest. These changes are probably pathologic and are amenable to pharmacologic intervention.