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Real-Time Monitoring of Extracellular Glutamate Release on Repetitive IschemicInjury in Global Ischemia Model

机译:实时监测重复缺血时细胞外谷氨酸的释放全球缺血模型中的伤害

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During the operation, neurosurgeons usually perform the multiple temporary occlusions of parental artery which may induce the neuronal damage. It is generally thought that neuronal damage by cerebral ischemia is associated with extracellular concentrations of the excitatory amino acids. In this experiment, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion (VO) model during repeated occlusion within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flow metry simultaneously with cortical glutamate level measured by am-perometric biosensor. During ischemic episode, the maximum change of glutamate release was gradually decreased as 112.38 ± 26.21 uM in first period, 82.63 ± 18.50 uM in second period, and 48.58 ± 11.89 uM in third period. The time interval between the ischemia induction and the beginning of glutamate release was increased as 106.7 ± 10.89 (sec) at first attack, 139.11 ± 3.87 (sec) in second attack, 169.00 ± 14.56 (sec) in third ischemic period. From the results of real-time monitoring about glutamate release in 11 VO model during repetitive ischemic episode, it was demonstrated that repetitive ischemia induced less glutamate release from neuronal cell than single ischemia due to endogeneous protective mechanism which delayed glutamate release time in later ischemic injury.
机译:在手术过程中,神经外科医生通常会执行多次临时性的父母亲动脉阻塞,这可能会引起神经元损伤。通常认为,脑缺血引起的神经元损伤与兴奋性氨基酸的细胞外浓度有关。在本实验中,我们在短时间间隔内反复进行闭塞期间,测量了11血管闭塞(VO)模型中细胞外谷氨酸释放的动力学。激光多普勒血流仪同时监测大脑血流量的变化,同时用安培生物传感器测量皮层谷氨酸水平。在缺血发作期间,谷氨酸释放的最大变化逐渐降低,第一阶段为112.38±26.21 uM,第二阶段为82.63±18.50 uM,第三阶段为48.58±11.89 uM。缺血诱导与谷氨酸释放开始之间的时间间隔在第一次发作时增加为106.7±10.89(sec),在第二次发作时增加为139.11±3.87(sec),在第三次缺血期增加为169.00±14.56(sec)。实时监测11 VO模型重复缺血发作期间谷氨酸释放的结果表明,与内源性保护机制相比,重复缺血诱导的神经元谷氨酸释放少于单次缺血,这是由于内源性保护机制延迟了谷氨酸释放在以后的缺血性损伤中的时间。 。

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