Monoamine oxidae-induced hydroxyl radical production and cardiomyocyte injury during myocardial ischemia-reperfusion

2016 Fiscal Year Final Research Report

• Project/Area Number: 26462774
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Emergency medicine
• Research Institution: National Cardiovascular Center Research Institute
• Principal Investigator: AKIYAMA Tsuyoshi 国立研究開発法人国立循環器病研究センター, 研究所, 室長 (70202554)
• Co-Investigator(Renkei-kenkyūsha): INAGAKI Tadakatsu 独立行政法人国立循環器病研究センター, 血管生理学部, 上級研究員 (20638366) ; SHIMIZU Shuji 独立行政法人国立循環器病研究センター, 循環動態制御部, 上級研究員 (80443498)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 心臓 / 虚血・再灌流 / モノアミン / ヒドロキシラジカル / マイクロダイアリシス法

Outline of Final Research Achievements

We applied microdialysis technique to the heart of anesthetized rats. Dialysate samples were collected during 30 min of induced ischemia followed by 60 min of reperfusion. We monitored dialysate 3,4-dihydrobenzoic acid (3,4-DHBA) concentration as an index of hydroxyl radical production using a trapping agent (4-hydroxybenzoic acid), and dialysate myoglobin concentration as an index of cardiomyocyte injury in the ischemic region. Dialysate 3,4-DHBA concentration increased during ischemia and further increased after reperfusion. Pargyline, a MAO inhibitor, suppressed the averaged increase in dialysate 3,4-DHBA concentration during ischemia and reperfusion. Dialysate myoglobin concentration increased during ischemia and further increased after reperfusion. Pargyline reduced the averaged dialysate myoglobin concentration during ischemia and reperfusion. MAO plays a significant role in hydroxyl radical production and cardiomyocyte injury during ischemia and after reperfusion.

Free Research Field

循環生理学