| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2012: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Outline of Final Research Achievements |
Left atrial (LA) thrombosis is an important cause of systemic embolization. The aim of the present study was to investigate how spontaneous model rats develop LA thrombi. Nitric oxide (NO) produced from cardiovascular endothelial cells plays an important protective role in blood flow, vascular tone, and platelet aggregation. No evidence of atrial fibrillation or hypercoagulability in the model rats regardless of age was found; however, the model rats demonstrated endothelial dysfunction and a decrease of NO production. In addition, endothelial NO synthase activity was significantly decreased in the LA and thoracic aorta endothelia of the model rats. However, L-arginine treatment significantly increased NO production and provided protection from the development of LA thrombi in the model rats. They present study results indicate that NO has an important role in the development of LA thrombus, and endothelial pathways could provide new targets of therapy to prevent LA thrombosis.
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