| Project/Area Number |
09670439
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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 |
Legal medicine
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| Research Institution | Asahikawa Medical College (1998)
Shimane Medical University (1997) |
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Principal Investigator |
UEZONO Takashi School of Medicine, Asahikawa medical college, Instructor, 医学部, 助手 (70294387)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUBARA Kazuo School of Medicine, Asahikawa medical college, Professor, 医学部, 教授 (20127533)
KIMURA Kojiro School of Medicine, Shimane medical university, Professor, 医学部, 教授 (30153191)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥2,100,000 (Direct Cost: ¥2,100,000)
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| Keywords | carbon monoxide poisoning / delayed neurodegeneration / pallidum / neuronal death / brain microdialysis / glutamate |
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| Research Abstract |
After a coma caused by carbon monoxide poisoning, complete amnesia is often followed by psychosis. In autopsy findings, degeneration of cerebral cortex and hippocampus is observed as well as transient ischemia. Pallidal necrosis is a characteristic finding in the carbon monoxide poisoning, but rare in the transient ischemia, On the other hand, carbon monoxide is suggested to function as a chemical mediator in the central nerve system. as like as nitric oxide. Therefore, the mechanism of cell death in carbon monoxide intoxication may be different from that of ischemia.
To clarify this, we measured extra cellular glutamate level in the rat pallidum with a microdialysis technique. Anesthetized male Wistar rats were stereotaxially implanted with 22-gauge cannulae in the left pallidum at AP - 0.9 mm, L + 2.8 mm from the bregma, and - 5.2 mm from the skull. The rats were housed in plastic cages (30 x 30 x 35 cm) and the air containing 1% carbon monoxide was flushed through the cage. Although glutamate levels were constant during the exposure to carbon monoxide, the extracellular glutamate levels were gradually elevated to 170% three hours after the exposure. In the microscopic study, neurons of cerebral cortex, the sommer sector and pallidum revealed to be ischemic changes the same as seen in ischemia induced by middle cerebral artery occlusion. Dark blue shriveled neurons were observed after staining with hematoxylin-eosin.
In contrast to the ischemia induced by middle cerebral artery occlusion and insulin-induced hypoglycemia, a delayed increase in glutamate levels was a characteristic feature. This result suggested that carbon monoxide might act as a chemical mediator to induce cell death in its poisoning.
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