Effects of subarachnoid and intravenous administration of lidocaine on glutamate concentration during cerebral ischemia in rats
| Project/Area Number |
07457347
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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 |
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) |
MIZUNUMA Takahide Akita Univ., School of Medicine, Instructor, 医学部, 助手 (50261665)
MASAKI Yoko Akita Univ., School of Medicine, Instructor, 医学部, 助手 (30125744)
TERADA Hiromichi Akita Univ., School of Medicine, Instructor, 医学部, 助手 (60282183)
岩崎 洋一 秋田大学, 医学部, 助手 (50282182)
秋山 博美 秋田大学, 医学部, 助手 (40261664)
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| Project Period (FY) |
1995 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥4,900,000 (Direct Cost: ¥4,900,000)
Fiscal Year 1997: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1996: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1995: ¥3,400,000 (Direct Cost: ¥3,400,000)
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| Keywords | Cerebral ischemia / Glutamate / Local anesthetic / Lidocaine / Microdialysis electrode / Subarachnoid administration / Intravenous administration / マイクロダイアリシス / 大脳皮質 / 海馬 / くも膜下腔 / くも膜下腔投与 |
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| Research Abstract |
It has been recognized that the accumulation of glutamate during cerebral ischemia may trigger the neuronal injury. We studied whether the pre-ischemic subarachnoid or intravenous administration of lidocaine would influence the rise of extracellular glutamate concentration during transient forebrain ischemia in rats, using the newly developed "dialysis electrode" method.
Exp.1 : Anesthetized rats were administrated lidocaine (5 mg/kg) or normal saline in the cisterna magna. Thereafter 10-min forebrain ischemia was induced by bilateral carotid arteries occlusion and hypotension. We monitored real-time changes of glutamate concentration by the dialysis electrodes implanted in cortex and hippocampal CAl simultaneously before and during ischemia, and reperfusion. As results, during ischemia, glutamate concentrations in these regions showed initial rapid rises, followed by persisting gradual increases during the remainder of ischemia. The maximum values of glutamate concentration in the cort
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ex were lower in the lidocaine group (n=9 ; 107(]SY.+-。[)44muM,mean(]SY.+-。[)SD ; P<0.05) than the saline group (n=9 ; 205(]SY.+-。[)126muM), while those in the hippocampal CAl were similar between groups. With the cession of ischemia, glutamate concentrations rapidly returned to the baselines. Exp.2 : Anesthetized rats were intravenously administrated lidocaine (10 mg/kg) or normal saline. As the first experiment protocol, glutamate concentrations in cortex and hippocampal CAl were measured during 10-min forebrain ischemia. As results, the maximum values of glutamate concentration in each region during ischemia were similar between groups.
The dose of lidocaine intravenously administrated in second study may fail to lead to the effective therapeutic concentration in the cerebral tissue. The accumulation of glutamate in the cortex during transient forebrain ischemia was attenuated by subarachnoid lidocaine. This finding suggests that lidocaine may act as a protective agent against transient cerebral ischemia. Less
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Report
(4 results)
Research Products
(8 results)
