Development of a new therapeutic strategy for preventing the cardiac ischemia/reperfusion injury based on the mechanisms underlying cardioprotective effects of volatile anesthetics

2017 Fiscal Year Final Research Report

• Project/Area Number: 26462336
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Anesthesiology
• Research Institution: Shiga University of Medical Science
• Principal Investigator: KOJIMA Akiko 滋賀医科大学, 医学部, 助教 (50447877)
• Co-Investigator(Kenkyū-buntansha): 北川 裕利 滋賀医科大学, 医学部, 教授 (50252391) ; 松浦 博 滋賀医科大学, 医学部, 教授 (60238962)
• Project Period (FY): 2014-04-01 – 2018-03-31
• Keywords: 心筋保護効果 / 心筋虚血再灌流傷害 / Ca2+輸送タンパク質 / TRPCチャネル / 心筋リアノジン受容体

Outline of Final Research Achievements

Intracellular Ca2+ overload during ischemia/reperfusion in myocardium is responsible for cellular injury leading to cardiac dysfunction, namely ischemia/reperfusion injury. Because various Ca2+ transport proteins, such as type 2 ryanodine receptor (RyR2) and store-operated Ca2+ entry (SOCE) channel, are involved in Ca2+ overload-induced cellular injury, we investigated whether blocking these channels is effective in reducing the cardiac ischemia/reperfusion injury.
In mouse hearts subjected to ischemia/reperfusion, contractile functions of left ventricle were significantly reduced compared with these baseline value. In contrast, administration of RyR2 blocker or SOCE channel blockers ameliorated the contractile dysfunction after ischemia/reperfusion. These results indicate that RyR2 and SOCE channel are involved in the development of cardiac ischemia/reperfusion injury and can provide the potential therapeutic targets to prevent the heart from ischemia/reperfusion injury.

Free Research Field

麻酔学