Yang Y, Li Q, Miyashita H, Yang T, Shuaib A
Department of Medicine, University of Alberta, Edmonton, Canada.
Neuropathology. 2001 Sep;21(3):181-7. doi: 10.1046/j.1440-1789.2001.00397.x.
The extent and severity of neuronal damage is different in ischemia with reperfusion compared to ischemia and no reperfusion. To investigate the role of glutamate in cerebral ischemia-reperfusion injury, in vivo microdialysis was performed to examine the dynamic profile of glutamate in the hippocampus in a transient (30 min) or permanent middle cerebral artery occlusion (MCAo) in Wistar rats. The extracellular concentration of glutamate in the cornu ammonis (CA)1 sector of the ipsilateral hippocampus showed a significant but transient elevation of glutamate for both groups immediately following ischemic insult. The initial high peak in glutamate levels in the transient MCAo group was followed by two secondary elevations in glutamate at 50 min and 90 min after initialization of reperfusion. The histopathological outcome was also different in the two groups. The observation that glutamate releases occurred in the early reperfusion phase provided an evidence of additional excitotoxicity of glutamate and thereby a therapeutic base for extended use of glutamate antagonist in the ischemia-reperfusion injury.
与缺血且无再灌注相比，缺血再灌注时神经元损伤的程度和严重性有所不同。为了研究谷氨酸在脑缺血再灌注损伤中的作用，采用体内微透析技术，检测Wistar大鼠短暂性（30分钟）或永久性大脑中动脉闭塞（MCAo）后海马中谷氨酸的动态变化。两组在缺血损伤后即刻，同侧海马角回（CA）1区细胞外谷氨酸浓度均显著但短暂升高。短暂性MCAo组谷氨酸水平最初的高峰之后，在再灌注开始后50分钟和90分钟出现了两次谷氨酸的二次升高。两组的组织病理学结果也不同。谷氨酸在再灌注早期释放这一观察结果，为谷氨酸的额外兴奋性毒性提供了证据，从而为在缺血再灌注损伤中扩大使用谷氨酸拮抗剂提供了治疗依据。
