The Effect of Extracellular Glutamate Release on Repetitive Transient Ischemic Injury in Global Ischemia Model.
10.4196/kjpp.2009.13.1.23
- Author:
Gi Ja LEE
1
;
Seok Keun CHOI
;
Yun Hye EO
;
Sung Wook KANG
;
Samjin CHOI
;
Jeong Hoon PARK
;
Ji Eun LIM
;
Kyung Won HONG
;
Hyun Seok JIN
;
Berm Seok OH
;
Hun Kuk PARK
Author Information
1. Department of Biomedical Engineering, School of Medicine, Kyunghee University, Seoul 130-702, Korea. sigmoidus@khu.ac.kr
- Publication Type:Original Article
- Keywords:
Repeated transient occlusion;
Real time monitoring;
Extracellular glutamate release
- MeSH:
Arteries;
Biosensing Techniques;
Brain Ischemia;
Excitatory Amino Acids;
Glutamic Acid;
Glycosaminoglycans;
Humans;
Ischemia;
Laser-Doppler Flowmetry;
Neurons;
Parents
- From:The Korean Journal of Physiology and Pharmacology
2009;13(1):23-26
- CountryRepublic of Korea
- Language:English
-
Abstract:
During operations, neurosurgeons usually perform multiple temporary occlusions of parental artery, possibly resulting in 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 study, we measured the dynamics of extracellular glutamate release in 11 vessel occlusion (VO) model to compare between single occlusion and repeated transient occlusions within short interval. Changes in cerebral blood flow were monitored by laser-Doppler flowmetry simultaneously with cortical glutamate level measured by amperometric biosensor. From real time monitoring of glutamate release in 11 VO model, the change of extracellular glutamate level in repeated transient occlusion group was smaller than that of single occlusion group, and the onset time of glutamate release in the second ischemic episode of repeated occlusion group was delayed compared to the first ischemic episode which was similar to that of single 10 min ischemic episode. These results suggested that repeated transient occlusion induces less glutamate release from neuronal cell than single occlusion, and the delayed onset time of glutamate release is attributed to endogeneous protective mechanism of ischemic tolerance.
