Pathlophysiological significance of intracellular calcium dynamics in the heart during ventricular fibrillation
Project/Area Number |
16590707
|
Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
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Research Institution | Kyoto Prefectural University of Medicine |
Principal Investigator |
TANAKA Hideo Kyoto Prefectural University of Medicine, Instructor, 医学研究科, 講師 (60236619)
|
Co-Investigator(Kenkyū-buntansha) |
TAKAMATSU Tetsuro Kyoto Prefectural University of Medicine, Professor, 医学研究科, 教授 (40154900)
|
Project Period (FY) |
2004 – 2005
|
Project Status |
Completed (Fiscal Year 2005)
|
Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
|
Keywords | ventricular fibrillation / calcium / gap junction / calcium wave |
Research Abstract |
This study was designed to clarify the role of intracellular calcium (Ca) dynamics of the heart in the maintenance of ventricular fibrillation (VF) in the perfused rat heart. Using in situ confocal microscopy and fluorescence vital miscopy in the fluo-3-loaded and di-4 ANEPPS-perfused rat heart, intracellular Ca dynamics and the mapping of the membrane potentials respectively were analyzed on the subepicardial surface of the heart. The results are as follows; 1)While the heart during sinus rhythm exhibited propagation from the apex to the base on excitation with a constant propagation velocity, the heart under VF exhibited inhomogeneous patterns of excitation showing spiral waves. 2)The heart during VF revealed inhomogeneous Ca dynamics including Ca waves and Ca alternans, which became more evident as the VF continued. 3)Application of ryanodine during maintained VF reduced or diminished Ca waves and Ca transients, but failed to attenuate VF. In contrast, verapamil improved the inhomogeneity of Ca dynamics and eventually the heart showed VT or sinus rhythm. These results indicated that VF promotes intracellular Ca overload, which could contribute to the maintenance of VF. However, Ca overload is unlikely to be a pivotal culprit factor in the maintenance of VF.
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Report
(3 results)
Research Products
(16 results)