| Project/Area Number |
08457306
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
General surgery
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| Research Institution | Ryukyu University |
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Principal Investigator |
KAMADA Yoshihiko (1997) Ryukyu University, Faculty of Medicine, Associate Professor, 医学部・附属病院, 講師 (10177561)
草場 昭 (1996) 琉球大学, 医学部, 教授 (40038659)
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| Co-Investigator(Kenkyū-buntansha) |
SAKUDA Hitoshi Ryukyu University, Faculty of Medicine, Associate Professor, 医学部・附属病院, 助手 (80244309)
鎌田 義彦 琉球大学, 医学部, 講師 (10177561)
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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 |
¥6,400,000 (Direct Cost: ¥6,400,000)
Fiscal Year 1997: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1996: ¥5,000,000 (Direct Cost: ¥5,000,000)
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| Keywords | autovein graft / endothelial cell / smooth muscle cell / intimal hyperplasia / shear stress / collagen / cell culture / vascular surgery / 細胞培養 / 術後晩期閉塞 / 仮性内膜肥厚 / 内皮細胞 / 末梢血管抵抗 |
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| Research Abstract |
The mechanism causing intimal hyperplasia at the anastomotic site in peripheral revascularization procedures, resulting in late graft failure, is obscure at the present time. This intimal hyperplasia occurs mostly in grafts with poor distal outflow, at regions of low shear stress. We studied the effects of shear stress on type IV and type IV collagen production by cultured canine vascular endothelial cells, using disk a rotation device. Semi-quantitative measurements on immunohistochemically processed samples were performed. We found that lower shear stress induced the endothelial cells to produce more type I and type IV collagen. Type IV collagen is a major component of the subendothelial basement membrane. Type I collagen occurs throughout the depth of the hyperplastic intima, and has been shown to promote modulation of cultured arterial smooth muscle cells from a contractile to a synthetic phenotype. We hypothesize that vascular endothelial cells can regulate subendothelial smooth muscle cell activity through control of collagen production in response to shear stress conditions. This mechanism might play an important role in the development intimal hyperplasia seen in the late postoperative period.
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