Role of iron ions in the genesis of reperfusion injury following successful cardiopulmonary resuscitation: preliminary data and a biochemical hypothesis.
Presented is a rationale for use of a new class of drugs, the iron chelating agents, in advanced cardiac life support (ACLS) to prevent late deaths and brain damage following successful cardiopulmonary resuscitation. The relevant biochemical hypothesis states that free iron ions, liberated from bound intracellular stores during ischemia, catalyze initiation of free radical mediated reactions that propagate through membrane lipids and proteins. Progressive ultrastructural damage may result, ultimately causing deterioration of function and death. Chelation of intracellular iron by deferoxamine, a commercially available drug that distributes to the intracellular space and has a great affinity for iron ions, may prevent such reactions. A hypothesis concerning relevant pathological chemistry is developed in detail.
D000818:Animals; D002545:Brain Ischemia / Q000188:drug therapy / Q000378:metabolism*; D003676:Deferoxamine / Q000627:therapeutic use; D005609:Free Radicals; D006323:Heart Arrest / Q000188:drug therapy*; D006801:Humans; D006900:Hydroxylation; D007477:Ions; D007501:Iron / Q000378:metabolism*; D008054:Lipid Peroxides / Q000378:metabolism; D009243:NAD / Q000378:metabolism; D051381:Rats; D012151:Resuscitation; D013482:Superoxide Dismutase / Q000378:metabolism
D005609:Free Radicals; D007477:Ions; D008054:Lipid Peroxides; D009243:NAD; D007501:Iron; D013482:Superoxide Dismutase; D003676:Deferoxamine