Prough D S, Kong D, Watkins W D, Stout R, Stump D A, Beamer W C
Stroke. 1986 Nov-Dec;17(6):1272-6. doi: 10.1161/01.str.17.6.1272.
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 PGF1 alpha (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 PGF1 alpha were significantly higher in treated animals at most post-ischemic intervals. CBF in both groups was similar to baseline values at time 0, then declined similarly in both groups by 30 min to approximately equal 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.
在全脑缺血的犬类模型中，6只犬在缺血事件发生前接受了选择性血栓素A2合成酶抑制剂UK 38,485（达唑麦角）；6只接受了生理盐水安慰剂。在基线、主动脉和腔静脉阻断解除后以及此后长达120分钟的间隔时间测量脑血流量（CBF）、收缩压和舒张压、心输出量、pH值、动脉血二氧化碳分压（PaCO2）、动脉血氧分压（PaO2）以及动脉和颈静脉血栓素B2（血栓素A2的稳定代谢产物）和6-酮前列环素F1α（前列环素的稳定代谢产物）。接受治疗的动物在缺血后血栓素B2生成几乎完全受到抑制；对照动物颈静脉血栓素B2升高。在大多数缺血后间隔时间，接受治疗的动物动脉和颈静脉6-酮前列环素F1α水平显著更高。两组的CBF在0时刻与基线值相似，然后两组在30分钟时均类似地下降至约为基线值的35%，此后维持在该水平。在任何间隔时间，其他变量均无显著差异。我们得出结论，抑制血栓素A2生成不会改变缺血后脑灌注不足。
