Several investigations have rekindled important concern that administration of 100% oxygen during and early after resuscitation from experimental cardiopulmonary arrest might be deleterious to the brain. In a canine model of ventricular fibrillation cardiopulmonary arrest, use of 100% oxygen compared with use of room air early during resuscitation was associated with increased neuronal death in selectively vulnerable brain regions and worse neurological outcome.1 Several studies have focused on oxidative injury to key mitochondrial enzymes (such as pyruvate dehydrogenase or manganese superoxide dismutase) or mitochondrial lipids (such as cardiolipin) in mediating these deleterious effects.2- 4
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