BIOMECHANICAL FACTORS IN ANASTOMOTIC INTIMAL HYPERPLASIA

动脉内膜增厚是正常愈合反应的一个特征 移植物吻合。然而，在移植到外周动脉时，内膜 吻合口远端的增生是主要原因。 人造血管移植失败。药理学上的努力 最大限度地减少小血管吻合口内膜增生 到目前为止，这一举措并不成功。这种方法不会直接 解决在远端占优势的生物力学因素 小血管的吻合术或血管内病变的性质 吻合口的流场。与血流动力学相关的因素 具有树枝几何形状，并具有 动脉壁与血管内膜的定位密切相关 增厚和动脉粥样硬化。血管吻合影响 改变几何形状、壁面顺应性的近壁流动特性 以及吻合口周围的运动和流速。 我们的工作假设是吻合口的分布 血管内膜增厚或增生的分布与 作用在流体-壁界面处的壁上的剪应力 主要发生在低切变和振荡切变区域 应力，即局部颗粒停留时间增加的情况。我们 因此建议在犬体内建立血管搭桥术。 在不同吻合口几何条件下，血流 调整墙特征，例如出现在 接受下肢动脉搭桥术的患者 以评估相关机械和机械设备的效果 构型因素对本土化程度的影响 愈合过程中吻合口内膜增厚 进程。为了实现这一点，我们将量化空间 用计算机检测吻合口内膜增厚的分布 辅助三维重建技术和 将这些发现与尺度上的空间分布联系起来 壁面剪应力与颗粒滞留时间的关系模型 到几何学，移植物对动脉顺应性和 吻合口周围血管的血流速度分布。这个 预计调查结果将明确和定量地定义， 第一次对吻合口周围的实际定位 血管内膜增厚和相应的流场条件， 并确定最佳的生物力学条件 最大限度减少吻合口内膜增生。

Intimal thickening is a feature of the normal healing response at graft anastomoses. Yet, in grafts to peripheral arteries, intimal hyperplasia at the distal anastomosis is the major cause of prosthetic vascular graft failure. Pharmacologic efforts to minimize intimal hyperplasia in small vessel anastomoses have thus far been unsuccesful. This approach does not directly address the biomechanical factors which prevail at distal anastomoses to small vessels or the nature of the changes in the flow field at anastomotic sites. Hemodynamic factors associated with branch geometry and with the mechanical properties of the artery wall correlate closely with the localization of intimal thickening and atherosclerosis. Vascular anastomoses affect near-wall flow properties by altering geometry, wall compliance and motion, and flow velocities about the anastomotic junction. It is our working hypothesis that the distribution of anastomotic intimal thickening or hyperplasia corresponds to the distribution of shear stress acting on the wall at the fluid-wall interface and occurs principally in regions of lowered and oscillartory shear stress, i.e., where local particle residence time is increased. We therefore propose to construct vascular bypass grafts in dogs under conditions of differing anastomotic geometry, flow conditions an wall characteristics such as those which occur in patients undergoing lower extremity arterial bypass surgery and to assess the effects of the associated mechanical and configurational factors on the localization and degree of anastomotic intimal thickening during the course of the healing process. To accomplish this we will quantify the spatial distribution of anastomotic intimal thickening using computer- assisted three dimensional reconstruction techniques and correlate these findings with the spatial distribution in scale models of wall shear stress and particle residence time in relation to geometry, to graft versus artery compliance and to the distribution of flow velocities in the perianastomatic vessels. The findings would be expected to define clearly and quantitatively, for the first time, the actual localization of perianastomotic intimal thickening and the corresponding flow field conditions, and to identify the optimal biomechanical conditions for minimizing anastomotic intimal hyperplasia.