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Anastomotic Stenosis is a Cause of Intimal Hyperplasia at the Middle Portion of Arterial Graft

Anastomotic Stenosis is a Cause of Intimal Hyperplasia at the Middle Portion of Arterial Graft
吻合口狭窄是移植动脉中部内膜增生的原因
批准号:
12671336
负责人:
OSAKO Motohiko
金额:
$2.18万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2000
资助国家:
日本
项目状态:
已结题
起止时间:
2000 至 2001

项目摘要

项目成果

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中文摘要
翻译
背景:动脉移植物已成为冠状动脉搭桥手术的首选材料。然而,动脉移植物的通畅取决于吻合的质量,吻合口狭窄是搭桥失败的原因之一。吻合口狭窄不仅在吻合口附近,而且在移植物的中间部分也可能通过改变内皮功能导致内膜增生(IH)。方法与结果:将新鲜制备的RT11大鼠胸主动脉移植至同种大鼠腹主动脉。对近端或远端吻合部位进行绑扎,使管腔大小为原移植物的50-75%。近端狭窄(PS)组(0.78+/-0.18)和远端狭窄(DS)组(0.53+/-0.03)与无狭窄(NS)组(0.19+/-0.09)相比,吻合口附近宿主腹主动脉流速(M/m2)与移植物中部的差异显著(p < 0.05)。PS组(48.3+/-6.7)和DS组(21.3+/-4.3)明显高于NS组(6.0+/-2.5)。各组狭窄程度与IH程度呈显著负相关。然而,在吻合口狭窄程度相同的情况下,PS产生的IH明显高于DS。免疫组化分析显示,PS组和DS组一氧化氮合酶3型(NOS3)阳性内皮细胞数量明显少于NS组。PS组nos3阳性内皮细胞明显少于PD组。结论:这些结果表明,动脉移植物的近端或远端吻合口狭窄是移植物中部IH的重要决定因素。然而,在吻合口狭窄严重程度相同的情况下,PS的IH程度比PD更突出。内皮细胞的一氧化氮合成受损与血流速度降低和其他未确定的机械力的调节有关,可能参与了这一发病机制。少
英文摘要
Background : Arterial grafts have become a choice of materials for coronary artery bypass surgery. However, patency of arterial grafts depends on the quality of anastomosis, and anastomotic stenosis is a cause of bypass failure. Anastomotic stenosis alterflow conditions within the grafts not only at the proximity of anastomosis but also at the middle portion of the graft that may leads to intimal hyperplasia (IH) by modifying endothelial functio. Methods and Results : Freshly prepared thoracic aorta from RT11 rats were transplanted to the abdominal aorta of the same strain. Proximal or distal anastomotic site was banded to create a luminal size of 50-75% of the original graft. The difference in flow velocity (M/m2) between the host abdominal aorta at the proximity of the anastomosis and the middle portion of the graft was significantly greater in proximal stenosis (PS) group (0.78+/-0.18) and in distan stenosis (DS) group (0.53+/-0.03) than in no-stenosis (NS) group (0.19+/-0.09). IH a … More s assessed by the ratio of intimal/medial are (%) at the middle portion of the graft 30 days after surgery was significantly reater in PS group (48.3+/-6.7) and in DS group (21.3+/-4.3) than in NS group (6.0+/-2.5). There was a significant negative correlation between the severity of stenosis and the degree of IH in each group. However, PS produced significantly greater IH compared with DS when the degree of anastomotic stenosis was identical. Immunohistochemical analysis revealed significantly less number of nitric oxide synthase type 3 (NOS3)-positive endothelial cells in PS and DS groups than in NS group. NOS3-positive endothelial cells were significantly less in PS group tha in PD group.Conclusions : These results suggest that anastomotic stenosis of arterial grafts either proximal or distal is an important determinant for IH at the middle portion of the graft. However, the degree of IH is more prominent in PS than in PD when the severity of anastomotic stenosis is identical. Impaired nitric oxide synthesis by endothelial cells associated with reduced flow velocity and modulation of other undertermined mechanical forces may be involved in this pathogenesis. Less
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会议论文
大迫茂登彦: "中枢側及び末梢側吻合部狭窄が自家動脈グラフトリモデリングに及ぼす影響"The Japanese Journal of Thoracic and Cardiovascular Surgery. 48(abstracta). 287 (2000)
Shigehiko Osako:“中央和远端吻合口狭窄对自体动脉移植物三边形的影响”《日本胸心血管外科杂志》48(摘要)。
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大迫 茂登彦, 他10名: "中枢側及び末梢側吻合部狭窄が自家動脈グラフトリモデリングに及ぼす影響"The Japanese Journal of Thoracic and Cardiovascular Surgery. 48(abstract). 287 (2000)
Shigetohiko Osako 等 10 人:“中央和远端吻合口狭窄对自体动脉移植物重塑的影响”,日本胸心血管外科杂志 48(摘要)。
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大迫茂登彦, 他10名: "吻合部狭窄は自家動脈グラフトのリモデリングを促進する"日本心臓血管外科学会雑誌.
Shigetohiko Osako 等人 10 人:“吻合口狭窄促进自体动脉移植物的重塑”日本心血管外科学会杂志。
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大迫 茂登彦, 他10名: "吻合部狭窄は自家動脈グラフトのリモデリングを促進する"日本心臓血管外科学会雑誌. 31(supplement). 16 (2001)
Shigetohiko Osako等10人:“吻合口狭窄促进自体动脉移植物的重塑”日本心血管外科学会杂志31(增刊)16(2001年)。
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共 6 条
    FK506, Denudation of Donor Endothelial Cells and Bafilomycin A_1, a Selective Inhibitor of Vacuolar H^+-ATPase, Inhibit Neointimal Hyperplasia in Rat Cryopreserved Aortic Allograft
    • 批准号:
      14571289
    • 项目类别:
      Grant-in-Aid for Scientific Research (C)
    • 资助金额:
      $2.11万
    • 财政年份:
      2002
    • 负责人:
      OSAKO Motohiko
    • 依托单位: