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Improvement of vasoactive dysfunction on rat cerebral penetrating arterioles in early brain injury after subarachnoid hemorrhage.

Research Project

Project/Area Number 16K10716
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Neurosurgery
Research InstitutionShinshu University

Principal Investigator

Murata Takahiro  信州大学, 医学部附属病院, 特任研究員 (80533322)

Project Period (FY) 2016-04-01 – 2020-03-31
Project Status Completed (Fiscal Year 2019)
Budget Amount *help
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords脳細動脈の機能障害 / くも膜下出血 / 早期脳障害 / カリウムチャンネル
Outline of Final Research Achievements

Early brain injury (EBI) after rupture of rupture inducing subarachnoid hemorrhage (SAH) is characterized by a severe reduction in cerebral blood flow suggesting alterations on the cerebral small vessels. In this early vascular injury on small vessels after SAH, vasoactive dysfunction via potassium channels is unclear. We investigated whether SAH induced immediate ATP-sensitive potassium (KATP) channels dysfunction in rat experimental SAH model, and free radical scavenger restored KATP channels dysfunction. To investigate the KATP channels function, the activator was applied with or without free radical scavenger. The vasodilatory responses to the activator were attenuated in SAH rats but not saline injection and sham surgery rats. Free radical scavenger-treated arteriolar dilatory response to the activator was partially restored compared with non-treated arteriolar response. KATP channels may inactivate immediately after SAH, and the dysfunction may be induced by free radical.

Academic Significance and Societal Importance of the Research Achievements

本研究の目的は,くも膜下出血(SAH)後の早期脳障害(EBI)による脳細動脈の血管調節機能の低下,とくにATP依存性カリウムチャンネルの機能低下を調査し,その機能が活性酸素捕捉薬で回復するか解明し,SAH後のEBIに対する有効な治療方法を開発することにある.結果,SAHのEBIにおいて脳細動脈のATP依存性カリウムチャンネルの機能障害が起きていると考えられ,その原因として活性酸素が一因と推測された.これらの結果は,特にSAH後のEBIの治療における活性酸素捕捉薬の臨床使用において基礎的な背景を補うと考えられる.

Report

(5 results)
  • 2019 Annual Research Report   Final Research Report ( PDF )
  • 2018 Research-status Report
  • 2017 Research-status Report
  • 2016 Research-status Report
  • Research Products

    (4 results)

All 2019 2017

All Presentation (4 results) (of which Int'l Joint Research: 2 results)

  • [Presentation] くも膜下出血後の早期脳障害における脳細動脈の機能障害の改善2019

    • Author(s)
      村田貴弘、堀内哲吉
    • Organizer
      第78回日本脳神経外科学会学術総会
    • Related Report
      2019 Annual Research Report
  • [Presentation] Improvement of vasoactive dysfunction on rat cerebral penetrating arterioles in early vascular injury after subarachnoid hemorrhage.2019

    • Author(s)
      Takahiro Murata, Tetsuyoshi Horiuchi
    • Organizer
      Neuroscience 2019
    • Related Report
      2019 Annual Research Report
    • Int'l Joint Research
  • [Presentation] くも膜下出血後の早期脳障害における脳細動脈の機能障害2019

    • Author(s)
      村田貴弘
    • Organizer
      第44回日本脳卒中学会学術集会
    • Related Report
      2018 Research-status Report
  • [Presentation] Vasodilation induced by pinacidil are attenuated in early vascular injury after subarachnoid hemorrhage on rat cerebral penetrating arterioles.2017

    • Author(s)
      Takahiro Murata, Tetsuyoshi Horiuchi, Kazuhiro Hongo
    • Organizer
      Neuroscience 2017
    • Related Report
      2017 Research-status Report
    • Int'l Joint Research

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Published: 2016-04-21   Modified: 2021-02-19  

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