During the operation, surgeons in neurosurgical area usually performed 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 within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. During ischemia, the peak level of glutamate release was gradually decreased as 112.38±26.21 μM in first period, 82.63±18.50 μM in second period, and 48.58±11.89 μM 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.
- Bioengineering Division
Changes in Extracellular Glutamate Release on Repetitive Transient Occlusion in Global Ischemia Model
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Lee, G, Choi, S, Kang, S, Choi, S, Park, J, Park, DH, Park, Y, Kim, K, Oh, B, & Park, H. "Changes in Extracellular Glutamate Release on Repetitive Transient Occlusion in Global Ischemia Model." Proceedings of the ASME 2009 Summer Bioengineering Conference. ASME 2009 Summer Bioengineering Conference, Parts A and B. Lake Tahoe, California, USA. June 17–21, 2009. pp. 603-604. ASME. https://doi.org/10.1115/SBC2009-206602
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