| Project/Area Number |
08671399
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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 |
General surgery
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| Research Institution | Kinki University Hospital |
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Principal Investigator |
KAMIISHI Hiroshi Kinki University Hospital, Department of Plastic surgery, Professor, 医学部, 教授 (40050512)
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| Co-Investigator(Kenkyū-buntansha) |
ISOGAI Noritaka Kinki University Hospital, Department of Plastic surgery, Associate Professor, 医学部, 助教授 (90203067)
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| Project Period (FY) |
1996 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1998: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1997: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | replantation / avulsion injury / Patency rate / Diabetes mellitus / 切断指再接着術 / 閉塞率 / 微小血管吻合 / 超音波トランジット血流計 / パワースペクトラム |
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| Research Abstract |
It is known that the avulsed vessels are prone to cause postoperative thrombosis, which lowers the survival rate of the replanted finger. Precise mechanism of the thrombosis formation is not yet investigated, however, endothelial damage caused by the avulsion force has been suspected. In order to elucidate where and how the vessel obstruction takes place, we investigated the luminal surface of the avulsed-vessel using scanning electron microscopy. Initial result revealed the formation of extensive serial intimal ring-like cracks at and around the point of avulsion.. Further morphological study using light microscopy revealed that the cracks were the disruptions of the endothelial cell layer as well as internal elastic lamina. Deep cracks reaching media layer often generated the vulve-like projection into the lumen, where thrombus formation was found. It is concluded therefore that the avulsed-vessel demonstrates multiple intimal cracks. Cause of the vascular occlusion was considered to be the morphological alteration of the luminal surface with the serial deep cracks into the medial layer and the vulve-like projections. In the research with the diabetic rats, avulsed-vessels in the OLETF diabetic model demonstrated higher longitudinal extensibility of the vessel and the areas and depth of the multiple cracks in the luminal surface were clearly expanded. Post-avulsion vascular patency was lowered. From these results, it is concluded that the diseased vessel with diabetes mellitus has higher potency to generate thrombosis due to its fragility of the vessel structure.
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