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

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45 Scopus citations


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), γ-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.

Original languageEnglish (US)
Pages (from-to)164-175
Number of pages12
JournalThe Neuroscientist
Issue number3
StatePublished - May 1995


  • Free radicals
  • Hypothermia
  • Neurotransmitters
  • Nitric oxide
  • Pharmacotherapy

ASJC Scopus subject areas

  • Neuroscience(all)
  • Clinical Neurology


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