Direct cardioprotective effect of dexmedetomidine against ischemia/reperfusion injury in hypertensive hypertrophied myocardium

Research Project

Project/Area Number	26861237
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Anesthesiology
Research Institution	Sapporo Medical University
Principal Investigator	Yoshikawa Yusuke 札幌医科大学, 医学部, 研究員 (40721759)
Research Collaborator	HIRATA Naoyuki
Project Period (FY)	2014-04-01 – 2017-03-31
Project Status	Completed (Fiscal Year 2016)
Budget Amount *help	¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000) Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000) Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000) Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywords	デクスメデトミジン / 虚血再灌流障害 / 高血圧 / イミダゾリン / 肥大心筋
Outline of Final Research Achievements	The present study revealed that dexmedetomidine maintains the direct cardioprotective effect against ischemia/reperfusion injury in hypertensive hypertrophied myocardium via different mechanism from normal healthy heart. Dexmedetomidine protects normal healthy heart through eNOS phosphorylation via alpha2 adrenoreceptor. On the other hand, the results of the present study revealed that the cardioprotective effect of dexmedetomidine in hypertensive hypertrophied myocardium is via imidazoline 1 receptor, which remains in normal expression level, not via alpha2 adrenoreceptor, which is up-regulated in hypertrophied myocardium. Furthermore, our data indicated that eNOS phosphorylation does not contribute to the cardioprotective effect of dexmedetomidine in hypertensive hypertrophied myocardium.