| Budget Amount *help |
¥3,780,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥180,000)
Fiscal Year 2007: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2006: ¥3,000,000 (Direct Cost: ¥3,000,000)
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| Research Abstract |
Atrial fibrillation is a life-threatening disease that increases a risk of thrombus formation and heart failure. There are many possible mechanisms for this arrhythmia such as ectopic automaticity, reentry, conduction failure, etc., and they have yet to be elucidated. Because the atrium is composed of multiple types of cells including cardiac myocytes, endothelial cells, fibroblasts, vascular smooth muscle cells and so on, imaging of cellular activities in original tissues seems to be appropriate means for studies of atrial arrhythmias. In this work, we visualized cellular activities in atrial tissues and studied the mechanisms of atrial fibrillation.
Atrial muscles were obtained from pig or guinea pig hearts and loaded with Rhod-2 and/or Di-4-ANEPPS. Two-dimensional fluorescence signals were obtained using a confocal microscope system. We found some distinct characteristics of atrial muscles. Firstly, in most of atrial muscles, Ca^<2+> waves occurred at the same time as initiation of action potential-induced Ca^<2+> transients. This means that delayed afterdepolarization (DAD)cannot occur in those myocytes. Instead, early afterdepolarization (EAD) may be a cause of triggered. Activity in most part of atrium. Secondly, Ca^<2+> transients often alternate within individual cells, which is in marked contrast to ventricular cells where Ca^<2+> transients alternated between cells but not within single cells. Because the alternans has been suggested to be a cause of abnormal conduction, the less EC coupling ability and frequent alternans may be reasons for high probability of reentry in atrium. Finally, the procedure developed here appeared to be also useful for studies of ventricular arrhythmia.
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