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

机译:全球性缺血模型重复缺血性损伤对细胞外谷氨酸抑制的实时监测

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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:在操作期间,神经外部通常进行父母动脉的多个临时闭塞,这可能会诱导神经元损伤。通常认为脑缺血的神经元损伤与细胞外浓度的兴奋性氨基酸有关。在该实验中,在短时间内,我们在重复闭塞期间测量了11个血管闭塞(VO)模型中细胞外谷氨酸释放的动态。通过激光 - 多普勒流动法测量脑血流量的变化,同时用am-rErometric Biosensor测量的皮质谷氨酸水平。在缺血集中,谷氨酸释放的最大变化逐渐减少为第一期为112.38±26.21 um,在第二个时期82.63±18.50 um,第三期,48.58±11.89um。缺血诱导和谷氨酸释放开始之间的时间间隔在第一次攻击时增加为106.7±10.89(秒),第二次攻击中的139.11±3.87(秒),第三个缺血期169.00±14.56(秒)。从对11 VO模型中的关于谷氨酸释放的实时监测结果,证明重复缺血诱导从神经元细胞的较少谷氨酸释放,而不是单缺血,由于内均缺血,延迟谷氨酸释放时间在后来的缺血性损伤中延迟。

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