Project/Area Number |
07671499
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Cerebral neurosurgery
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Research Institution | Chiba University School of Medicine |
Principal Investigator |
YAMAURA Akira Chiba University School of Medicine, Chairman and Professor, Department of Neurosurgery, 医学部, 教授 (40009717)
|
Co-Investigator(Kenkyū-buntansha) |
YAMAKAMI Iwao Chiba University School of Medicine, Lecturer, 医学部, 講師 (90241968)
岡 信男 千葉大学, 医学部, 講師 (40114251)
|
Project Period (FY) |
1995 – 1996
|
Project Status |
Completed (Fiscal Year 1996)
|
Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1995: ¥1,800,000 (Direct Cost: ¥1,800,000)
|
Keywords | experimental brain injury / intentional changes of brain temperature / heat shock protein / hypothermia / immunohistochemistry / glial response / 実験的脳挫創 |
Research Abstract |
In this project, we investigated the effects of intentional changes of brain temperature on the experimental brain contusion. Firstly as a preliminary study, in 1995, we evaluated the immunohistochemical expression of 72 kDa heat shock protein (HSP72) as a marker of neuronal damage. Adult male rats were subjected to a lateral fluid percussive injury. Injured rats were divided into two groups ; normothermic group (37.0-37.5゚C) and hypothermic group (30.0-31.5゚C). The immunohistochemical evaluation was performed at 24,48, and 72 hours after injury. The results showd that HSP72-positive neurons were observed most prominently at 24 hours in both groups but their numbers in hypothermic group were significantly less than those in normothermic group. This preliminary study suggested that the protective effects of moderate hypothermia on the injured brain. According to these results, in 1996, we made a plan to evaluate the effects of intentional changes of brain temperature on blood-brain barrier (BBB) disruption and glial response. However, after the completion of the preliminary study in 1995, some problems which disturbed the next plan occured : 1) The breakdown of fluid percussive injury device and vibratome. 2) Unexpected non-specific background staining in immunohistochemisty. 3) Technical problems such as new cooling-heating method and insertion of epidural thermosenser into posterior fossa. 4) The possibility of difference in brain injury formation between old (1995) and new (1996) injury model. As a result, among 22 treated rats, we could evaluate only three rats (34゚C group=2,37゚C group=1) concerning to expression of HSP72 and glial response at 24 hours after injury. The results showed that there were no obvious effects of mild hypothermia (34゚C) on expression of HSP72 and microglial activation, whereas astrocytic responses were seemd to decrease in mild hypothermic group.
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