1997 Fiscal Year Final Research Report Summary
The role of excitatory amino acids in cellular injury following localized brain hyperthermia
| Project/Area Number |
07671523
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Yamaguchi Univeristy |
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Principal Investigator |
ITO Haruhide Yamaguchi Univ.School of Med.Professor, 医学部, 教授 (90019927)
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| Co-Investigator(Kenkyū-buntansha) |
FUJISAWA Hirosuke Yamaguchi Univ.School of Med.Assistant, 医学部, 助手 (50238565)
MAEKAWA Tsuyoshi Yamaguchi Univ.School of Med.Professor, 医学部, 教授 (60034972)
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| Project Period (FY) |
1995 – 1997
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| Keywords | hyperthermia / excitatory amino acid / microdialysis / cerebral blood flow / cerebral glucose use / autoradiography / protein kinase C / rat |
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| Research Abstract |
Purpose : The purpose of this study was to clarify the mechanisms in volved in cellular injury caused by hyperthermia in the central nverous system (CNS). For this purpose, the changes in the extracellular concentration of the excitatory amino acid glutamate, cerebral blood flow, local cerebral glucose use and second messenger system following localized hyperthermia were investigated.
Methods : Adulmale Wistar rats were used. (1) Sequential changes in the extracellular glutamate concentrations were measured using brain microdialysis following hyperthermia induced by the heating lump system. (2) Suquential changes in cortical cerebral blood flow (CBF) following hyperthermia following radiofrequency (RF) ^<-3> induced localized hyperthermia were measured. (3) Local cerebral glucose use were measured using [^<14>C] -2-deoxyglucose (DG) autoradiography following RF-induced hyperthermia. (4) Distribution of proteinkinase C (PKC) were measured using [^3H] phorbol 12,13-dibutyrate ([^<>H-PDBu)
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autoradiography following RF-induced hyperthermia.
Results : The extracellular glutamate concentration was not increased by mild hyperthermia (41ﾟC), but it increased remarkably by moderate (43ﾟC) hyperthermia. The elevated glutamate concentrations reached neurotoxic levels. In the cortex heated to 41ﾟC,the CBF doubled after hyperthermiainduction and returned to the prehyperthermic level. In the cortex heated to 43ﾟC,the CBF transiently increased after hyperthermiainduction, and then fell gradually to reach to 31% of the baseline level. In the cortex heated to 45ﾟC,the CBF decreased immediately after hyperthermia induction to reach 10% of the baseline level. LCGU markedly decreased in the areas heated to 45ﾟC,and it markedly increased in the areas heated to 43ﾟC.The increases in LCGU were also observed in some areas of the contralateral hemisphere. Low values of the PKC activities were observed in the ipsilateral hemisphere and in some areas in the contralateral hemisphere.
Conclusion : The results indicate that hyperthermia-induced cellular injury in the CNS is associated with cerebral ischaemia and a glutamate-mediated "excitotoxic" process. The changes in glucose metabolism and PKC activities following hyperthermia are similar to those in cerebral ischemia. The results obtained in this study will provide important information for clinical application of hyperthermia. Less
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Research Products
(6 results)
