Cell culture study on the mechanism and control of late graft failure occuring in arterial reconstruction procedures.

在外周血管重建术中，导致吻合口内膜增生，从而导致晚期移植失败的机制目前尚不清楚。这种内膜增生主要发生在远端流出不良的移植物中，在低切应力的区域。我们利用圆盘旋转装置研究了切应力对培养的犬血管内皮细胞产生IV型和IV型胶原的影响。对免疫组织化学处理后的标本进行半定量检测。我们发现较低的剪切力诱导内皮细胞产生更多的I型和IV型胶原。IV型胶原是内皮下基底膜的主要成分。I型胶原存在于增生性内膜的整个深度，并已被证明促进培养的动脉平滑肌细胞从收缩表型向合成表型的转变。我们假设，血管内皮细胞可以通过控制胶原蛋白的产生来调节内皮下平滑肌细胞的活性，以响应剪应力条件。这一机制可能在术后晚期内膜增生的发生发展中起重要作用。

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.