The study of mechanisms and prevention of arrhythmogenetic remodeling of ventricular myocardium caused by oxidative stress under hyperglycemic state.

2015 Fiscal Year Final Research Report

• Project/Area Number: 25461071
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Cardiovascular medicine
• Research Institution: Tamagawa University
• Principal Investigator: HIROE Niwano 玉川大学, 教育学部, 教授 (00293233)
• Co-Investigator(Kenkyū-buntansha): NIWANO Shinichi 北里大学, 医学部, 准教授 (70282978)
• Project Period (FY): 2013-04-01 – 2016-03-31
• Keywords: 酸化ストレス / SOD欠損マウス / 不整脈基盤 / 糖尿病

Outline of Final Research Achievements

In this study, hyperglycemic state was induced by the injection of streptozotocin (STZ) in heart/muscle-specific manganese superoxide dismutase-hetero deficient (H/M-Sod2+/-) mice and the myocardial electoro-physiological status was evaluated. In this model mice, we documented the hyper-production of reactive oxygen species(ROS) and the electrical remodeling which characterized by prolongation in ERP and MAPD with the increase of inducibility of ventricular arrhythmia. Also, EUK-8 (the SOD/catalase mimetic) treatment diminished the ROS production independently to the hyperglycemic condition, and suppressed these electoro-physiological changes. This result may indicate the importance of oxidative stress in promotion of the electrical remodeling in acute hyperglycemic state.

Free Research Field

循環器内科学