SUMMARY In a canine model of global brain ischemia, six dogs received a selective thromboxane A 2 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, PaCO 2 , PaO 2 , and arterial and jugular-vein thromboxane B 2 (a stable metabolite of thromboxane Aj) and 6-keto PGF ln (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 B 2 production; control animals showed increases in jugular venous thromboxane B 2 . Arterial and jugular venous levels of 6-keto PGF, a 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 A 2 production does not alter post-ischemic brain hypoperfusion.