| Project/Area Number |
07671524
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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 |
FUJISAWA Hirosuke Yamaguchi Univ.School of Med.Assistant, 医学部, 助手 (50238565)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Haruhide Yamaguchi Univ.School of Med.Professor, 医学部, 教授 (90019927)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥300,000 (Direct Cost: ¥300,000)
Fiscal Year 1996: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | head injury / cerebral contusion / excitatory amino acids / glutamate / hypothermia / cerebral blood flow / microdialysis / hypoxia / 低血圧 / 外傷性脳損傷 / ラット |
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| Research Abstract |
Purpose : The purpose of this study was to investigate the effects of hypothermia on the release of the excitatory amino acids (EAAs) and cerebral blood flow (CBF) during cerebral contusion. The effects of hypothermia on hypoxia-induced changes in the amino acids were also investigated.
Methods : Adult male Wistar rats were used. The animals were devieded two experimental groups : normothermia group (37ﾟC) and hypothermia group (32ﾟC). Cerebral contusion was created in the parietal cortex by a weight-drop method. (1) CBF was monitored using the hydrogen clearance technique, and cortical levels of EAAs were measured by intracerebral microdialysis. (2) Cerebral hypoxia (PaO2 : 30-40 mmHg) was induced for 60 min. CBF was measured by laser-Doppler flowmetry, and the extracelular concentrations of EAAs were measured by microdialysis. (3) After cerebral contusion was created, hypoxia was induced. CBF and the EAA concentrations were measured by the same methods as (2).
Results : (1) CBF in both
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groups decreased significantly after contusion but never fell below the threshold for ischemia. Cortical levels of EAAs were significantly increased after contusion in each group. However, these increases were greater in the hypothermic than in the normothermic rats. (2) Arterial blood pressurefell markedly during hypoxia in both groups, and returned to the normal range after cessation of hypoxia. CBF showed modest increases during hypoxia in both groups. Mild hypothermia abolished the EAA surge seen under norjmothermic conditions. (3) EAA levels were significantly increased after contusion in each group, and these increases were greater in the hypothermic than in the normothermic rats as the experiment (1). The EAA levels of the normothermic animals increased again after hypoxia induction. Mild hypothermia abolished such hypoxia-induced EAA surge.
Conclusion : Hypothermic cerebroprotection in traumatic brain injury (TBI) is likely to occur through a kmechanism other than reduction in interstitial excitatory amino acids. It is postulated that the postsynaptic effects of hypothermia may be more important than the presynaptic effects, when CBF is kept above the ischemic threshold. Cerebral hypoxia contributes to the complex spectrum of pathology of TBI.The results of these study suggest that secondary damage caused by cerebral hypoxia can be ameliorated by hypothermia. Less
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