| Project/Area Number |
05671247
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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 | Akita University |
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Principal Investigator |
OHTA Sukejuro Akita Univ., School of Medicine, Assistanat professor, 医学部, 講師 (90125708)
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| Co-Investigator(Kenkyū-buntansha) |
MASAKI Yoko Akita Univ., School of Medicine, Instructor, 医学部, 助手 (30125744)
水沼 隆秀 秋田大学, 医学部, 医員(臨床医)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | Cerebral ischemia / Delayd neuronal death / Local anesthetic / Lidocaine / Subarachnoid administration / Spreading depression / Hypoxia / Cerebral protection / くも膜下腔注入 / 遅発性神経細胞壊死 |
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| Research Abstract |
We investigated whether the pre-ischemic subarachnoid administration of lidocaine can reduce post-ischemic delayd neuronal damage. Anesthetized rats were administrated normal saline or lidocaine (5 mg/kg) in cistern magna. Thereafter forebrain ischemia for ten minutes was made by bilateral clamp of carotid arteries and hypotension. Brains were perfusion-fixed 7 days after recovery and stained with celestine blue/acid fuchsin. Results : The number of delayd neuronal death in cerebral cortex and hippocampus CA4 was significantly less in lidocaine group than in control group. However, there were no significant differences in the degree of neuronal damage in hippocampus CA1 and caudoputamen in both groups.
The second study was designed to explore whether cortical spreading depression (SD) is related to the occurrence of delayd neuronal death. SD was elicited by the epidural application of KCL in the right forehead, when cortical DC potential was detected with a micro-glass electrode placed
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in the ipsilateral parietal cortex. Rats were undergone the clamp of the right carotid artery (CCA) or hypoxia for 2-3 hours. Brains were fixed 7 days after recovery. Results : There was no neuronal damage in brains which suffered only SD,only hypoxia, SD+hypoxia, or hypoxia+CCA.However there was mild neuronal damage in the ipsilateral cerebral cortex which suffered hypoxia+CCA+SD.
In cerebral ischemia, Ca^<2+> influx is accelerated by the depolarization of postsynaptic membrane. Lidocaine has an inhibition of depolarization by blocking Na^+ channel. The first study suggests that the ameliorative reduction of postischemic delayd neuronal damage after the subarachnoid administration of lidocaine is contributed to the inhibition of depolarization by the cortical infiltration of lidocaine and the inhibition against the perforating fibers' projection for hippocampus. The second study implies that the postischemic detrimental process for delayd neuronal damage may need not only cerebral hypoperfusion and hypoxia but also severe spreading depolarization of synaptic membrane. Less
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