Cardiac gap junction and pacemaker cells in alcoholic sudden cardiac death
| Project/Area Number |
22590635
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Legal medicine
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| Research Institution | Yamaguchi University |
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Principal Investigator |
LIU Jinyao 山口大学, 大学院・医学系研究科, 講師 (60379956)
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| Co-Investigator(Kenkyū-buntansha) |
FUJIMIYA Tatsuya 山口大学, 大学院医学系研究科, 教授 (50219044)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | アルコール医学 / 致死的不整脈 / 心筋線維形成 / 心筋ギャップ結合 / アルコール / 突然死 / 交感神経活性化 / 心臓性突然死 / 心筋ギャップ結合リモデリング / 心筋線維化 / 心筋ギャップ結合機能 |
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| Research Abstract |
The influences of myocardial fibrosis and gap junction remodeling on the alcoholic life-threatening ventricular arrhythmias were evaluated in rats, particularly in acute ethanol withdrawal rats. Acute ethanol withdrawal followed 49-day continuous ethanol treatment induced a high risk of myocardial fibrosis formation; down-regulation of gap junction protein connexin (Cx) 43 protein and mRNA expressions; down-regulation of phosphorylated Cx43 protein expression; however, all of them were normalized by carvedilol (can block the sympathetic nervous system completely via β1, β2, and - adrenergic receptors) pretreatment. Acute ethanol withdrawal followed 49-day continuous ethanol treatment is sufficient to increase the risk of myocardial fibrosis formation and gap junction remodeling via the shift of cardiac sympathovagal balance toward sympathetic predominance, and then leads to the onset of the life-threatening ventricular arrhythmias in alcoholic subjects.
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Report
(4 results)
Research Products
(20 results)
