| Project/Area Number |
06671529
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | Yamaguchi University |
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Principal Investigator |
NAKAKIMURA Kazuhiko Yamaguchi University, Hospital Assistant Professor, 医学部・附属病院, 講師 (50180261)
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| Co-Investigator(Kenkyū-buntansha) |
SANO Takanobu Yamaguchi University, Hospital Research Associate, 医学部・附属病院, 助手 (40243670)
ISHIKAWA Toshizo Yamaguchi University, School of Medicine Research Associate, 医学部, 助手 (90034991)
SAKABE Takefumi Yamaguchi University, School of Medicine Professor, 医学部, 教授 (40035225)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | acute subdural hematoma / NMDA antagonist / brain injuries / rat / 硬膜下血腫 / 頭蓋内圧 / 脳代謝 / 脳循環 / 脳浮腫 / 血液脳関門 |
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| Research Abstract |
Using a rat model of acute subdural hematoma (150mul), we examined neurological consequences for 7 days after the insult. Most of rats recovered and moved actively for a couple of hours after the production of subdural hematoma. However, neurologically deteriorated thereafter and about a half of animals died within 48 hours after hematoma. The remaing rats survived 7 days and recovered nealy normal, although histological examination revealed cerabral infarction under the hematoma in these rats. In order to dintinguish the biochemical effects of thesubdural hematoma from the mass effects, the same volume (150mul) of inert silicone gel was injected into the subdural space and brains were perfused and fixed at 8 hours after the subdural injection for the subsequent histopathological examination. The infarct volume was significantly smaller in rats received subdural injection of silicone compared with rats received subdural hematoma.
Conceming therapeutic interventions for acute subdural hematoma, we examined the effects of cerebral perfusion pressure and possibly effective medications including gabexate mesilate, MK-801, and ketamine.Among these treatments, only the effects of cerebral perfusion pressure was significant. In rats whose cerebral perfusion pressure was maintained above 80 mmHg with dopamine infusion during production of subdural hematoma, neurological scores at 4 and 7 days after hematoma were significantly better than those in rats without blood pressure support by dopamine infusion. The volume of cerebral infarct at 8 hours after hematoma was numerically reduced by treatment of MK-801.
In conclusion, the present study suggests exacerbation of brain damages due to diffusible substances from the subdural hematoma, which could be inhibited by treatment of NMDA antagonists, and importance of maintenance of relatively high cerebral perfusion pressure during the management of acute subdural hematoma.
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