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Review : Neuroprotection in Brain Ischemia: An Update (Part II

Cerebral Vascular Disease Research Center Department of Neurology University of Miami School of Medicine Miami, Florida

Ischemic brain injury produced by stroke or cardiac arrest is a major cause of human neurological disability. Steady advances in the neurosciences have elucidated the pathophysiological mechanisms of brain ischemia and have suggested many therapeutic approaches to achieve neuroprotection of the acutely ischemic brain that are directed at specific injury mechanisms. In the second portion of this two-part review, the following potential therapeutic approaches to acute ischemic injury are considered: 1) modulation of nonglutamatergic neurotransmission, including monoaminergic systems (dopamine, norepinephrine, serotonin), -aminobutyric acid, and adenosine; 2) mild-to-moderate therapeutic hypothermia; 3) calcium channel antagonism; 4) an tagonism of oxygen free radicals; 5) modulation of the nitric oxide system; 6) antagonism of cytoskeletal proteolysis; 7) growth factor administration; 8) therapy directed at cellular mediators of injury; and 9) the rationale for combination pharmacotherapy. The Neuroscientist 1:164-175, 1995

Key Words: KEY WORDS Neurotransmitters • Hypothermia • Free radicals • Nitric oxide • Pharmacotherapy

The Neuroscientist, Vol. 1, No. 3, 164-175 (1995)
DOI: 10.1177/107385849500100307


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