Involvement of store-operated calcium entry in ischemia/reperfusion injury in the heart

2015 Fiscal Year Final Research Report

• Project/Area Number: 25460287
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General physiology
• Research Institution: Shiga University of Medical Science
• Principal Investigator: Matsuura Hiroshi 滋賀医科大学, 医学部, 教授 (60238962)
• Co-Investigator(Kenkyū-buntansha): KOJIMA Akiko 滋賀医科大学, 医学部, 助教 (50447877) ; TOYODA Futoshi 滋賀医科大学, 医学部, 助教 (90324574)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 虚血再灌流傷害 / 容量性カルシウム流入機構 / Ca2+過負荷 / 筋小胞体 / リアノジン受容体 / 2-APB / フレカイニド / ランゲンドルフ灌漑

Outline of Final Research Achievements

The present investigation provides experimental evidence to support that the store-operated Ca2+ entry (SOCE) is involved in ischemia/reperfusion injury in the heart. For example, in Langendorff-perfused mouse heart model, reperfusion following 30 min of global ischemia was associated with contractile dysfunction such as elevation of left ventricular end-diastolic pressure and reduction of left ventricular developed pressure. These dysfunctions were partially but significantly attenuated by the SOCE blockers 2-aminoethoxydiphenyl borate (2-APB) and LaCl3. In addition, flecainide, which blocks Ca2+ leak through type2 ryanodine receptor and thereby preserves Ca+ content in SR, was also effective in preventing the contractile dysfunction associated with ischemia/reperfusion injury in the heart. These observations suggest that the drugs that block Ca2+ leak from SR have protective effects against ischemia/reperfusion injury in the heart.

Free Research Field

心臓生理学