| Project/Area Number |
06671172
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Tokyo Women's Medical College |
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Principal Investigator |
NAKAZAWA Makoto Tokyo Women's Medical College, Dept of Pediatr Cardiol, Professor, 医学部, 教授 (10075567)
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| Co-Investigator(Kenkyū-buntansha) |
MORISHIMA Masae Tokyo Women's Medical College, Research Division, Assistant, 医学部, 助手 (00241068)
YASUI Hiroshi Tokyo Women's Medical College, Dept of Develop Biology, Assistant, 医学部, 助手 (60210241)
TOMITA Sachiko Tokyo Women's Medical College, Dept of Pediatr Cardiol, Assistant, 医学部, 助手 (40231451)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1995: ¥400,000 (Direct Cost: ¥400,000)
Fiscal Year 1994: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Keywords | Cardiac Anomaly / Mouse Embryo / Retinoic Acid / Transposition of the Great Arteries / Hemodynamics |
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| Research Abstract |
We had been trying to make a good model of transposition of the great arteries (TGA) in the mouse by treating pregnant dams by all-trans retinoic acid, and finally established the model in which TGA was induced in 90% of embryos by giving the drug with a dose of 70mg/kg at 8.5 days of gestation. Using this model, we have found that hypo-dysplasia of proximal outflow swelling causes failure of the normal ventriculo-arterial ralation and leads to parallel connection of the ventricles to the great arteries, i.e.the right ventricle (RV) to the aorta (Ao) and the left ventricle (LV) to the pulmonary artery (PA). We have then considered that it is important to find the role of hemodynamics in its morphogenesis, and established the technique in which the mammalian embryo is observed in situ under a microscope and action of the heart is recorded with a high speed video camera while it is still alive and viable. Using this method, it was found that there was two pattaerns of flow through outflow tract of the primitive ventricle in TGA model embryos ; one is that flow from RV to Ao was parallel to and separated from it from LV to PA ; the other was that flow from RV goes into both Ao and PA.The latter likely destined to TGA associated with malalign type ventricular septal defect, or double outlet right ventricle in an extreme case. Analysing the ventricular size and function, RV was smaller and lower in ejection fraction in TGA embryos than in controls, suggestings some possible role of hemodynamics in pathogenesis of TGA.
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