Fredriksson K, Rosén I, Johansson B B, Wieloch T
Stroke. 1985 Sep-Oct;16(5):800-5. doi: 10.1161/01.str.16.5.800.
Platelet aggregating sodium arachidonate was slowly infused into the internal carotid artery (1 mg, 100 microliters, 1 microliter/s) of nitrous oxide anesthetized rats. The electroencephalographic activity recorded by a Cerebral Function Monitor from the injected hemisphere was reduced within minutes. The somatosensory evoked responses to contralateral electrical stimulation of the whisker area were eliminated on the same side in most cases when measured five and fifteen minutes after the infusion. The brain was frozen in situ with liquid nitrogen after fifteen minutes. Regional tissue analysis showed ipsilateral derangement of the cerebral energy state and increased lactate levels. Pretreatment with the platelet antiaggregating thromboxane synthetase inhibitor OKY-1581 (Sodium-3-4-(3-pyridylmethyl)phenyl-2-methyl-acrylate), 30 mg/kg i.v., fifteen minutes before the sodium arachidonate infusion prevented cerebral energy failure and elimination of the sensory evoked responses.
将花生四烯酸钠缓慢注入氧化亚氮麻醉大鼠的颈内动脉（1毫克，100微升，1微升/秒）。通过脑功能监测仪记录的来自注射半球的脑电图活动在数分钟内降低。在注入后5分钟和15分钟测量时，大多数情况下，对触须区域对侧电刺激的体感诱发电位在同侧消失。15分钟后用液氮将脑原位冷冻。区域组织分析显示同侧脑能量状态紊乱，乳酸水平升高。在注入花生四烯酸钠前15分钟静脉注射血小板抗聚集血栓素合成酶抑制剂OKY - 1581（3 - 4 -（3 - 吡啶基甲基）苯基 - 2 - 甲基丙烯酸酯钠）30毫克/千克，可预防脑能量衰竭和感觉诱发电位的消失。
