Effects of nimodipine on the production of thromboxane A2 following total global cerebral ischemia

W. S. Haddon, D. S. Prough, D. Kong, P. Petrozza

Research output: Contribution to journalArticle

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Abstract

To clarify the contribution of vasoconstrictor prostaglandins to the hypoperfusion state typically following total global cerebral ischemia, 14 mongrel dogs were subjected to 11 minutes of global cerebral ischemia. They were then randomly assigned to receive either no treatment or an intravenous bolus of the calcium channel blocker nimodipine, 10 μg/kg, 15 minuts after ischemia followed by a continuous infusion of nimodipine, 1.0 μg/kg/min. Thromboxane (Tx) A2 production, as measured by cerebral venous levels of TxB2 (the stable metabolite of TxA2) increased similarly in the two groups. In contrast to previous studies, mean postischemic cerebral blood flow did not increase sufficiently in the nimodipine-treated group to achieve statistical significance. These data suggest that the improved neurological outcome associated with nimodipine treatment following global cerebral ischemia does not relate to reduced levels of the prostaglandin precursor arachidonate.

Original languageEnglish (US)
Pages (from-to)416-420
Number of pages5
JournalJournal of neurosurgery
Volume69
Issue number3
DOIs
StatePublished - Jan 1 1988

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ASJC Scopus subject areas

  • Surgery
  • Clinical Neurology

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