1999 Fiscal Year Final Research Report Summary
Effects of cerebral hypothermia on brain tissue impedance and extracellular ion concentrations
| Project/Area Number |
10671320
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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 | Juntendo University |
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Principal Investigator |
MORI Kentaro Juntendo University, Dep of Neurosurgery, Assistant Profesor, 医学部, 助教授 (30200364)
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| Co-Investigator(Kenkyū-buntansha) |
KUSUMOTO Masayuki Juntendo University, Dep of Neurosurgery, Assistant, 医学部, 助手 (20195449)
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| Project Period (FY) |
1998 – 1999
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| Keywords | hypothermia / cerebral ischemia / glutamate / vasoconstriction / brain impedance / extracellular ion / water channel / ion channel |
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| Research Abstract |
The purpose of this research project was to investigate the protective mechanismas of cerebral hypothermia and to improve its therapeutic effects.
1. Effects of cerebral hypothermia on cerebral blood flow and metabolism
We investigated the effects of hypothermia on cerebral blood flow (CBF) and metabolism (CMROィイD22ィエD2, AVDOィイD22ィエD2), cerebral venous oxygen saturation (ScvOィイD22ィエD2), cerebral blood volume (CBV), and cerebral vascular resistance (CVR) using 34 anesthetized cat. Brain temperature was controlled from 37 to 25℃. AVDOィイD22ィエD2 increased significantly at 29℃, ScvOィイD22ィエD2 decreased significantly at 29℃, CBV decreased significantly at 29℃, and CVR increased significantly at 29℃. The combined effect of hypothermia with vasopressor (noradrenalin) administration improved all these metabolic parameters. These results suggest that hypothermia below 30℃ may cause cerebral vasoconstriction and misery perfusion in the brain. This potential risk of relative ischemia can be avoided b
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y combination with vasopressor administration.
2. Effects of cerebral hypothermia on brain tissue impedane and extracellular ion concentrations
We investigated the effects of mild cerebral hypothermia on brain tissue impedance (brain extracellular space: ECS) and extracellular ion concentrations ([NaィイD1+ィエD1] ィイD2eィエD2, [KィイD1+ィエD1] ィイD2eィエD2) under cerebral ischemia using anesthetized 11 rats. After global ischemia, ECS began to decrease (post-ischemic cell swelling) at 32±5 sec and then [NaィイD1+ィエD1] ィイD2eィエD2 started to decrease (NaィイD1+ィエD1 ion influx into cells) at 83±30 sec. Hypothermia significantly prolonged both changes of ECS and extracellular ion concentrations. These result shows that cerebral ischemic cell swelling start to occur earlier than extracellular NaィイD1+ィエD1 ion influx into cells. This fact makes it difficult to explain the mechanism of the cell swelling by the former theory that swelling is caused by isotonic water movement after NaィイD1+ィエD1 influx. It is suggested that a depletion of intracellular ATP causes dephospholization of water channel (aquaporin 4) and directly open this water channel. Cerebral hypothermia may influence this water channel directly and prolong the opening of this water channel. Less
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