| Project/Area Number |
08671717
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | NIIGATA UNIVERSITY |
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Principal Investigator |
TAGA Kiichiro Niigata University Hospital Lecturer, 医学部・附属病院, 講師 (00163329)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIWARA Naoshi Niigata University Hospital Lecturer, 医学部・附属病院, 講師 (70181419)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Cerebral Ischemia / Ischemic Tolerance / Spreading Depression / Anesthetics / Intracellular Free Calcium / Glutamate |
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| Research Abstract |
(1) We investigated the producing condition of "Spreading Depression (SD)" by which ischemic tolerance is achieved. SD was generated by electrical stimulation in much weakerstimuli than those which have reported before. There is possibility that no response period exists just after the generation of SD.(2) We investigated the influences of anesthetics on the frequency, amplitude and latency of SD.Inhalational anesthetics decreased the frequency and extended the latency of SD according to the depth of anesthetics. Inhalational anesthetics did not affect the amplitude of SD.Ketamine, an NMDA antagonist, completely abolished the induction of SD.These data suggest that the NMDA receptor takes part in the generation of SD.The generation of SD was affected by the anesthetics itself and depth of it. (3) The concentrations of extracellular glutamate and intracellular calcium were measured in rats brain slices. The unilateral hemispheric transient depolarization (SD) were induced one day before the measurements of concentrations. There were no significant differences in both concentrations between SD and non-SD hemisphere during the oxygen-glucose deprivation. These results suggest the mechanism of ischemic tolerance induced by SD is not resulted from the increase of intracellular calcium during ischemia. (4) We evaluated the influences of anesthetics on the induction of ischemic tolerance. The preischemic SD was induced under ketamine or isoflurane anesthesia. One, three or seven days after SD,rats were subjected to forebrain ischemia. Injury to the cortex was evaluated in brain sections three days after ischemia. Preischemic SD that was induced under isoflurane anesthesia reduced postischemic injury. Ketamine anesthesia group did not improve the postischemic neuronal outcome. These data suggest that the NMDA receptor during the transient depolarization (SD) plays a central role in the acquisition of ischemic tolerance.
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