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pubmed-article:2180714pubmed:abstractTextCalcium antagonists are of potential value in preventing neuronal death following cerebral ischemia or anoxia. Prevention of calcium influx into neurons, not just preservation of cerebral blood flow, is necessary if these agents are to be protective. To be of value clinically in humans, these agents must be effective even if administered after the ischemic insult has occurred. Experimental studies suggest that flunarizine, which inhibits calcium influx following brain anoxia, prolongs clinical survival and prevents neuronal death even when administered after the ischemic event, has no known significant toxic effects in humans following acute administration, has important potential value in the treatment of stroke, and should be evaluated in controlled clinical trials of patients with acute stroke.lld:pubmed
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pubmed-article:2180714pubmed:authorpubmed-author:CohanS LSLlld:pubmed
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pubmed-article:2180714pubmed:volume30 Suppl 2lld:pubmed
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pubmed-article:2180714pubmed:pagination28-30; discussion 39-41lld:pubmed
pubmed-article:2180714pubmed:dateRevised2005-11-16lld:pubmed
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pubmed-article:2180714pubmed:articleTitlePharmacology of calcium antagonists: clinical relevance in neurology.lld:pubmed
pubmed-article:2180714pubmed:affiliationDepartment of Neurology, Georgetown University School of Medicine, Washington, D.C.lld:pubmed
pubmed-article:2180714pubmed:publicationTypeJournal Articlelld:pubmed
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