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

2019 Fiscal Year Final Research Report

• Project/Area Number: 16K10716
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Neurosurgery
• Research Institution: Shinshu 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
• Keywords: 脳細動脈の機能障害 / くも膜下出血 / 早期脳障害

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.

Free Research Field

脳神経外科

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．