Inhibition of thromboxane a2 production does not improve post-ischemic brain hypoperfusion in the dog

Donald S. Prough, Daniel Kong, W. David Watkins, Robert Stout, David A. Stump, Wilson C. Beamer

Research output: Contribution to journalArticle

11 Scopus citations

Abstract

In a canine model of global brain ischemia, six dogs received a selective thromboxane A2 synthetase inhibitor, UK 38,485 (dazmagrel) before the ischemic event; six received a saline placebo. Cerebral blood flow (CBF), systolic and diastolic arterial pressure, cardiac output, pH, PaCO2, PaO2, and arterial and jugular-vein thromboxane B2 (a stable metabolite of thromboxane A2) and 6-keto PGF1a (a stable metabolite of prostacyclin) were measured at baseline, after release of aortic and venae caval occlusion and at intervals up to 120 min thereafter. Treated animals showed nearly complete post-ischemic inhibition of thromboxane B2 production; control animals showed increases in jugular venous thromboxane B2. Arterial and jugular venous levels of 6-keto PGF1a were significantly higher in treated animals at most post-ischemic intervals. CBF in both groups was similar to baseline values at tune 0, then declined similarly in both groups by 30 min to ?35% of baseline values where it remained thereafter. There were no significant differences in other variables at any interval. We conclude that inhibition of thromboxane A2 production does not alter post-ischemic brain hypoperfusion.

Original languageEnglish (US)
Pages (from-to)1272-1276
Number of pages5
JournalStroke
Volume17
Issue number6
DOIs
StatePublished - Jan 1 1986
Externally publishedYes

ASJC Scopus subject areas

  • Clinical Neurology
  • Cardiology and Cardiovascular Medicine
  • Advanced and Specialized Nursing

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