Project/Area Number |
23591075
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
|
Research Institution | Hokkaido University |
Principal Investigator |
|
Project Period (FY) |
2011-04-28 – 2015-03-31
|
Project Status |
Completed (Fiscal Year 2014)
|
Budget Amount *help |
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2011: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
|
Keywords | 心房細動 / 伸展活性化チャネル / 高血圧 / 糖尿病 / 膜電位光学マッピング / カルシウムカルモジュリン依存性タンパク質キナーゼ / ギャップジャンクション / 循環器・高血圧 |
Outline of Final Research Achievements |
As a hypertensive experimental animal, spontaneously hypertensive rats (SHR) were used. Using the Langendorff-perfused hearts, elevation of left atrial pressure did not increase the inducibility of atrial fibrillation in SHR compared to normotensive Wistar-Kyoto rats (WKY). On the other hand, the CaMKII autophosphorylation, which has been reported to play an important role in the genesis of atrial fibrillation, was significantly increased in SHR. In addition to hypertension, diabetes mellitus (DM) is an independent risk of atrial fibrillation. Therefore, DM was induced by streptozotocin in WKY. The duration of atrial tachyarrhythmia was longer in DM. The conduction velocity (CV) was decreased, and its heterogeneity was greater in DM. Average action potential duration of 80% repolarization (APD(80)) from four areas within the RA was prolonged, and the coefficient of variation of APD(80) was greater in DM than control, indicating the possible substrate for atrial fibrillation.
|