BRAIN PROTECTION AGAINST ISCHEMIC-INJURY BY NIZOFENONE

Ischemic brain injury is induced in a complex and multifactorial patho genic cascade; but the fundamental mechanism is the imbalance between energy demand and supply in ischemic brain tissue. Nizofenone is a pot ent neuroprotective drug which ameliorates this imbalance and also var ious pathophysiologic events during ischemia, such as ATP depletion, l actate accumulation, glutamate release, free fatty acid liberation, ed ema, and neuronal degeneration; in particular, ischemia-induced excess ive glutamate release has been completely blocked by this drug. This d rug has also radical-scavenging action, comparable to vitamin E, and i nhibits oxygen radical-induced lipid peroxidation. The potent cerebrop rotective effect of nizofenone has been demonstrated in various experi mental models of cerebral hypoxia, ischemia (focal and global), ischem ia-reperfusion, and infarction. The clinical efficacy of nizofenone ha s been proved by pioneering double-blind studies in acute subarachnoid hemorrhage patients. Nizofenone is clinically used for preventing the delayed ischemic neurologic deficits due to late vasospasm following subarachnoid hemorrhage. In this report, the property of the cerebropr otective effect and the clinical efficacy of nizofenone is reviewed.