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大鼠大脑中动脉短暂闭塞后,对其半暗带皮质中水杨酸羟化作用和谷氨酸释放进行同步测量。

Simultaneous measurement of salicylate hydroxylation and glutamate release in the penumbral cortex following transient middle cerebral artery occlusion in rats.

作者信息

Morimoto T, Globus M Y, Busto R, Martinez E, Ginsberg M D

机构信息

Department of Neurology, University of Miami School of Medicine, Florida 33101, USA.

出版信息

J Cereb Blood Flow Metab. 1996 Jan;16(1):92-9. doi: 10.1097/00004647-199601000-00011.

Abstract

Using the microdialysis technique and laser-Doppler flowmetry, we performed simultaneous measurement of salicylate hydroxylation and glutamate release along with local CBF in the ischemic penumbral cortex of rat brain subjected to normothermic transient middle cerebral artery (MCA) occlusion. Cortical CBF fell to 24 +/- 11% (mean +/- SD) during ischemia and recovered to 84 +/- 16% during reperfusion. Extracellular glutamate levels increased by 6.5-fold above baseline 10 min following MCA occlusion but subsequently returned to near baseline levels in spite of the persistent ischemia. Increase in 2,3- and 2,5-dihydroxybenzoic acid (DHBA) concentrations in the microdialysis perfusate was confirmed during both ischemia and reperfusion phase. Although the temporal profile and amount of salicylate hydroxylation were heterogeneous among individual animals, integrated 2,3-DHBA concentrations during reperfusion were correlated positively with integrated glutamate concentrations during ischemia and negatively with mean postischemic CBF. These relationships suggest a possible association of the enhanced production of 2,3-DHBA during reperfusion with larger amounts of intraischemic glutamate release and lower levels of post-ischemic CBF.

摘要

我们采用微透析技术和激光多普勒血流仪,在常温下短暂大脑中动脉(MCA)闭塞的大鼠脑缺血半暗带皮层中,同步测量水杨酸盐羟化、谷氨酸释放以及局部脑血流量(CBF)。缺血期间皮层CBF降至24±11%(平均值±标准差),再灌注期间恢复至84±16%。MCA闭塞后10分钟,细胞外谷氨酸水平比基线升高6.5倍,但尽管缺血持续,随后仍恢复至接近基线水平。在缺血和再灌注阶段均证实微透析灌流液中2,3 - 二羟基苯甲酸(DHBA)和2,5 - 二羟基苯甲酸浓度增加。尽管个体动物之间水杨酸盐羟化的时间特征和量存在异质性,但再灌注期间2,3 - DHBA的综合浓度与缺血期间谷氨酸的综合浓度呈正相关,与缺血后平均CBF呈负相关。这些关系表明再灌注期间2,3 - DHBA生成增加可能与缺血期间大量谷氨酸释放及缺血后较低的CBF水平有关。

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