| Project/Area Number |
09470304
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Kurume University |
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Principal Investigator |
SHIGEMORI Minoru Medical Department, Kurume University, Professor, 医学部, 教授 (00080804)
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| Co-Investigator(Kenkyū-buntansha) |
MIYAGI Kazufumi Medical Department, Kurume University, Assistant, 医学部, 助手 (40268909)
YAMAGUCHI Shintaro Medical Department, Kurume University, Assistant, 医学部, 助手 (20289458)
TOKUTOMI Takashi Medical Department, Kurume University, Associate Professor, 医学部, 助教授 (90197872)
ISHIKAWA Kazufumi Medical Department, Kurume University, Assistant, 医学部, 助手 (70289461)
田口 明 久留米大学, 医学部, 助手 (40258439)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥11,600,000 (Direct Cost: ¥11,600,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1997: ¥10,600,000 (Direct Cost: ¥10,600,000)
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| Keywords | severe head injury / hypothermia / intracranial pressure / cerebral hemodynamics / cerebral metabolism / microdialysis |
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| Research Abstract |
We studied the effect of hypothermia on cerebral and systemic hemodynamics and metabolism in patients with severe head injury. Hypothermia was used only for the patients with a Glasgow Coma Scale score of ≦ 5. Patients were excluded from therapeutic hypothermia if they suffered from heart disease, coagulopathy, or hypotension and if their age were over than 70 years. All hypothermic patients were sedated, paralyzed, ventilated, and cooled to 32 to 33℃. Intracranial pressure (ICP), cerebral perfusion pressure (CPP), jugular bulb oxygen saturation (SjO2), mixed venous oxygen saturation (Svo2), cardiac output (CO), and whole body resting energy expenditure (REE) were continuously monitored. Changes in concentration of exitatory amino acids, glutamate (GLU) and NO were studied esing intracerebral microdialysis as well as in jugular venous blood and cerebrospinal fluid. Surface brain temperature was always higher than those at the jugular bulb, pulmonary artery, and rectum, commonly by 0.5℃. Hypothermia at temperature below 36℃ reduced IPC and increased CPP. SjO2 increased slightly and kept normal range during hypothermia. REE and CO decreased linearly with hypothermia, whereas SvO2 was constant. The concentration of GLU and NO significantly decreased at brain temperature 36℃ or below.
These results suggest that, after traumatic brain injury, hypothermia can improve intracranial hypertension and the uncoupling between blood flow and metabolism which commonly exists following severe head injury. However, 38% of the hypothermic patients died and only 21% had favorable outcome. Improvement of management for hypothermic patients is needed to cope with a adverse effect of hypothermia.
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