2022 Fiscal Year Final Research Report
Pharmacologial methods to inhibit pulmonary vein automaticity
| Project/Area Number |
20K07091
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Review Section |
Basic Section 47040:Pharmacology-related
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| Research Institution | Toho University |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Keywords | myocardium / diastolic depolarization / atrial fibrillation / late sodium current / sodium calcium exchanger / ectopic pacemaker / intracellular calcium |
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| Outline of Final Research Achievements |
Atrial fibrillation, which often leads to cerebral infarction, is a disease with a high need for treatment. At present, however, therapeutic agents with sufficient efficacy and safety is lacking. The goal of this study is to form a basis for the pharmacological treatment of atrial fibrillation. Using isolated pulmonary vein myocardium, the major site of the trigger for atrial fibrillation, we found two novel mechanisms for diastolic depolarization, the persistent Na current flowing through voltage dependent Na channels, and the Na-Ca exchanger current activated by intracellular Ca oscillation. Further studies for a novel drug usage and therapeutic agents are now in progress.
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| Free Research Field |
Cardiovascular Pharmacology
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| Academic Significance and Societal Importance of the Research Achievements |
心房細動は心房が細かく震える不整脈の一種であり、心房内で出来た血栓が脳梗塞を誘発するため治療必要性が極めて高い。現状では治療の中心は血栓予防薬および外科的手法による心房の興奮予防であり、細動自体を治療する薬理学的手段は確立されていない。心房細動の根本原因は心房から続く肺静脈心筋の電気的自発活動であり、これを抑制する仕組みの解明と、薬物治療や創薬につなげることの意味は大きい。
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