| Project/Area Number |
08671420
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Digestive surgery
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| Research Institution | NIIGATA UNIVERSITY |
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Principal Investigator |
UCHIDA Katsuyuki Niigata University Medical Hospital, Assistant, 医学部・附属病院, 助手 (50260542)
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| Co-Investigator(Kenkyū-buntansha) |
TSUKADA Kazuhiro Toyama Medical and Pharmaceutical University, faculty of medicine, Professor, 医学部, 教授 (90171967)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1997: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1996: ¥1,000,000 (Direct Cost: ¥1,000,000)
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| Keywords | liver regeneration / partial hepatectomy / portal pressure / rats / shear stress / 門脈圧亢進症 / 肝臓免疫 / 肝不全 / 肝免疫 |
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| Research Abstract |
The concept of injury regeneration after partial hepatectomy(PHx), and the reason hepatocytes that have not been directly injured regenerate, remain unclear, It is known that shear stress resulting from blood flow plays an important role in the mechnism of remodeling blood vessels, and portal pressure reflects shear stress. This study was conducted to determine whether acute portal hypertention(APH) can become a trigger of liver regeneration as shear stress following PHx in a rat model. Portal pressures became elevated immediately after 70% and 90% PHx, peaking on postoperative day (POD)3, and thereafter decreasing in proportion to the diminution of liver regeneration. The portal pressures after 90% PHx were significantly higher than those after without 70% PHx even on POD7. The gradient expressions of class I antigen on sinusoidal endothelial cells(SEC) were found only in the periportal area, which has the highest portal pressure in the healthy rat liver. However, after hepatectomy these expressions were detected from the periportal area tothe central venous area. These results suggest that APH as shear stress following PHx may not only become a trigger of hepatocyte regeneration, but also of SEC regeneration, and that surplus APH induces liver dysfunction.
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