1995 Fiscal Year Final Research Report Summary
Effects of shear stress on the intimal hyperplasia of autogenous Vein grafts
| Project/Area Number |
05807107
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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 |
General surgery
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| Research Institution | Second Department of Surgery, Faculty of Medicine, Kyushu University |
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Principal Investigator |
KOMORI Kimihiro Second Department of Surgery, Faculty of Medicine, Kyushu University (Assistant Professor), 医学部, 講師 (40225587)
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| Co-Investigator(Kenkyū-buntansha) |
KUMA Sosei Second Department of Surgery, Faculty of Medicine, Kyushu University (Medical st, 医学部, 医員
KAWASAKI Katsumi Second Department of Surgery, Faculty of Medicine, Kyushu University (Medical st, 医学部, 医員
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| Project Period (FY) |
1993 – 1995
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| Keywords | vein graft / intimal thickening / shear stress / prostacyclin / nitric oxide / eicosapentanoic acid |
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| Research Abstract |
Late graft failure is still a significant problem particularly in cases with poor runoff (low shear stress) vessels. We have already reported that the intimal thickening of the autogenous vein graft in the poor runoff model was significantly thicker than that in normal flow group. Endothelium modulates the responsiveness of the underlying vascular smooth muscles by releasing prostacyclin or endothelium-derived relaxing factor <Nitric Oxide (NO) >. These factor are not only vasodilators but also potent inhibitors of platelet aggregation. The present experiments were desingned to examine whether the production of prostacyclin or NO were altered in poor runoff conditions of canine autogenous vein grafts by using a poor runoff model. Under abnormal flow conditions characterized by low shear stress, the production of prostacyclin in the canine vein graft was lower than that in normal flow conditions. In addition, the production of NO in canine vein grafts are also impaired under poor runoff conditions.
Marine oils and high levels of eicosapentanoic acid (EPA) prevents intimal thickening in vein grafts. However, the precise mechanism by which EPA prevents intimal thickening is still unknown. The present experiments was designed toexamine whether EPA supplementation would alter the NO production in reversed vein grafts of dogs. The presents results demonstrated that EPA supplementation reduces intimal thickening of the autogenous vein graft, which may be due to an improved release of NO.
These results suggest that the dysfunction of the endothelium in terms of the decreased production of prostacyclin or NO under abnormal flow conditions may thus increase platelet aggregation and eventually facilitate the development of peripheral arterial occlusive disease and thus the occurrence of late graft failure. The preserved or enhanced endothelial function may be important role for preventing the late graft failure.
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