Ischemic-Anoxia of the Central Nervous System: Iron Dependent Oxidative Injury during Reperfusion

摘要

The work was begun with the recognition that the current practice of resuscitation from cardiac arrest due to either medical or traumatic causes results in major neurologic injury in 50-80% of resuscitated patients. Only in the last 25 years has there begun to be a systematic examination of the pathophysiology and molecular biology attendant to brain ischemia and reperfusion. The present work continues to examine the sequence of critical events in brain ischemia and reperfusion and tests therapies which may be applied during the reperfusion phase to inhibit the development of biochemical and functional markers of irreversible brain injury. The major products of this work are significant advances in the understanding of the pathophysiology of brain ischemia and reperfusion. During this period, flunarizine (calcium antagonist) and choloropromazine (effects in myocardium include inhibition of both phospholipase and of lipid peroxidation) for protective effects across the injury parameters were examined. Neither flunarizine nor chloropromazine have so far exhibited marked protective effects.