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The mechanism of axonal injury and regeneration after intrathecal administration of local anesthetics

Research Project

Project/Area Number 13671585
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeSingle-year Grants
Section一般
Research Field Anesthesiology/Resuscitation studies
Research InstitutionYamaguchi University

Principal Investigator

MATSUMOTO Mishiya  Yamaguchi Univ. Hospital, Assistant Professor, 医学部附属病院, 講師 (60243664)

Co-Investigator(Kenkyū-buntansha) SAKABE Takefumi  Yamaguchi Univ. School of Medicine, Professor, 医学部, 教授 (40035225)
FUKUDA Shirou  Yamaguchi Univ. Hospital, Research Associate, 医学部附属病院, 助手 (70322245)
IIDA Yasuhiko  Yamaguchi Univ. Hospital, Research Associate, 医学部附属病院, 助手 (90304485)
Project Period (FY) 2001 – 2002
Project Status Completed (Fiscal Year 2002)
Budget Amount *help
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2002: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2001: ¥2,000,000 (Direct Cost: ¥2,000,000)
KeywordsNeurotoxicity / local anesthetics / glutamate / apoptosis / oligodendrocyte / rabbit / 脊椎麻酔 / 脊髄
Research Abstract

High concentrations of local anesthetics have been known to be neurotoxic. However, the mechanism for their neurotoxicity Is obscure. We have reported that high concentrations of tetracaine administered intrathecally in the spinal cord increase glutamate concentrations and cause neuronal injury in a dose dependent manner. We investigated whether this is true in other local anesthetics and whether an AMPA receptor antagonist (YM872) can reduce neuronal injury caused by high concentrations of local anesthetics.
Lidocaine (10%) , tetracaine (2%), bupivacaine (2%), and ropivacaine (2%) were administered intrathecally at the cauda equina level to the rabbits implanted with an intrathecal microdialysis probe at the lumbar spinal cord level. Glutamate concentrations in the lumbar spinal cord level were monitored by microdialysis. Neurologic and histologic assessment was done one week after the administration. The peak concentrations of glutamate after lidocaine, tetracaine, bupivacaine, and ropivacaine were 10-fold, 6-fold, 5-fold, and 2.5-fold greater than baseline values, respectively. The degree of neuronal injury was in order of lidocaine > tetracaine > bupivacaine > ropivacaine.
Intrathecal administration of YM872 tended to reduce sensory and motor function at one week after administration of tetracaine. A chromatolytic change of the motor neuron caused by tetracaine was attenuated by YM872.
These results suggest that increased concentrations of glutamate in the cerebrospinal fluid is the common p phenomenon after intrathecal administration of local anesthetics and that glutamate plays, at least in part, an role in the mechanism of neurotoxicity by local anesthetics

Report

(3 results)
  • 2002 Annual Research Report   Final Research Report Summary
  • 2001 Annual Research Report
  • Research Products

    (2 results)

All Other

All Publications (2 results)

  • [Publications] Yamashita A, Matsumoto M, et al.: "A comparison of the neurotoxic effects on the spinal cord of tetracaine, lidocaine, bupivacaine, and ropivacaine administered intrathecally in rabbits"Anesthesia & Analgesia. (in press).

    • Description
      「研究成果報告書概要(和文)」より
    • Related Report
      2002 Final Research Report Summary
  • [Publications] Yamashita A., Matsumoto M., et al.: "A comparison of the neurotoxic effects on the spinal cord of tetracaine, lidocaine, bupivacaine, and ropivacaine administered intrathecally in rabbits"Anesthesia & Analgesia. in press.

    • Description
      「研究成果報告書概要(欧文)」より
    • Related Report
      2002 Final Research Report Summary

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Published: 2001-04-01   Modified: 2016-04-21  

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