Kochanek P M, Dutka A J, Hallenbeck J M
Stroke. 1987 May-Jun;18(3):634-7. doi: 10.1161/01.str.18.3.634.
Six anesthetized dogs treated with indomethacin, prostacyclin (PGI2), and heparin were compared with 7 anesthetized controls (ischemia without treatment) to determine whether cyclooxygenase inhibition would lead to enhanced granulocyte accumulation because of preferential formation of lipoxygenase products. Cortical somatosensory evoked response, [14C]iodoantipyrine autoradiographic blood flow, and 111In-labelled granulocyte accumulation were compared 4 hours after a 60-minute exposure to multifocal brain ischemia. Treatment with indomethacin, PGI2, and heparin eliminated neuron-disabling brain blood flows without altering early postischemic granulocyte accumulation. Granulocyte accumulation after 4 hours of reperfusion was not significantly different in control and treated dogs. The final amplitude of the cortical somatosensory evoked response in the treated group averaged 38.0 +/- 13.6% (mean +/- SEM) of the corresponding baseline value compared with 21.0 +/- 4.6% in the control group, but this difference was not significant.
将六只接受消炎痛、前列环素(PGI2)和肝素治疗的麻醉犬与七只麻醉对照组(未经治疗的缺血组)进行比较,以确定环氧化酶抑制是否会由于脂氧合酶产物的优先形成而导致粒细胞积聚增加。在暴露于多灶性脑缺血60分钟后4小时,比较皮质体感诱发电位、[14C]碘安替比林放射自显影血流以及111In标记的粒细胞积聚情况。消炎痛、PGI2和肝素治疗消除了导致神经元功能丧失的脑血流,而未改变缺血后早期的粒细胞积聚。再灌注4小时后,对照组和治疗组犬的粒细胞积聚无显著差异。治疗组皮质体感诱发电位的最终波幅平均为相应基线值的38.0 +/- 13.6%(平均值 +/- 标准误),而对照组为21.0 +/- 4.6%,但这一差异不显著。