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

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 micrograms/kg, 15 minutes after ischemia followed by a continuous infusion of nimodipine, 1.0 micrograms/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.
AuthorsW S Haddon, D S Prough, D Kong, P Petrozza
JournalJournal of neurosurgery (J Neurosurg) Vol. 69 Issue 3 Pg. 416-20 (Sep 1988) ISSN: 0022-3085 [Print] UNITED STATES
PMID3404240 (Publication Type: Journal Article)
Chemical References
  • Thromboxane A2
  • Nimodipine
  • Animals
  • Brain Ischemia (blood, drug therapy)
  • Cerebrovascular Circulation (drug effects)
  • Dogs
  • Nimodipine (therapeutic use)
  • Thromboxane A2 (blood)

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