ANASTOMOTIC INTIMAL HYPERPLASIA - MECHANICAL INJURY OR FLOW INDUCED

ANASTOMOTIC INTIMAL HYPERPLASIA - MECHANICAL INJURY OR FLOW INDUCED
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DOI:
10.1016/0741-5214(92)90019-5
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发表时间:
1992-04-01
影响因子:
4.3
通讯作者:
ZARINS, CK
ZARINS, CK
中科院分区:
医学2区
文献类型:
--
作者:
BASSIOUNY, HS;WHITE, S;ZARINS, CK

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所有吻合口内膜增厚可能不相同,调节不同类型的潜在机制可能不同。我们研究了实验性吻合口内膜增厚与已知生物力学和血流动力学因素的关系。在13只杂种犬中植入双侧髂股大隐静脉和聚四氟乙烯移植物。对远端端侧吻合几何形状进行标准化,并测量血流参数。8周后,10只动物中的7只(第1组)被处死,并通过灌注固定移植物。采用光学显微镜对每个吻合口的组织切片进行研究,并使用显微眼科学对内膜增厚区域进行识别和定量。为了表征吻合流模式,从三只动物(第11组)的远端吻合口铸件构建透明硅胶模型,并在模拟体内脉动流参数的条件下使用氦氖激光照射颗粒可视化血流。组织学切片显示两个独立且不同的吻合口内膜增厚区域。第一,缝合线内膜增厚,在聚四氟乙烯动脉瘤中(0.35 +/- 0.23 μ m)大于静脉动脉瘤(0.35 +/- 0.23 μ m)。15 +/- 0.03 μ-m,p < 0.05)。第二种不同类型的内膜增厚发生在动脉底部,在聚四氟乙烯(0.11 +/- 0.11-μ m)和静脉闭塞(0.12 +/- 0.03-μ m)中相同。模型血流可视化研究显示,沿动脉底沿着存在一个血流停滞点,导致出现第二种类型内膜增厚的低剪切和振荡剪切区域。沿着移植物的罩(没有内膜增厚的区域)观察到高剪切力和短颗粒停留时间。相对低剪切和长颗粒停留时间的区域形成沿着侧壁和足跟的血管,并没有特别相关的内膜增厚的缝合线。我们的结论是,至少存在两种不同类型的吻合口内膜增厚。缝合线内膜增厚代表血管愈合;假体移植物更突出可能与顺应性不匹配有关。动脉底内膜增厚与移植物类型无关,发生在血流振荡和相对低剪切的区域。在任一情况下,响应与改变的流动条件相关联。预防由闭塞性内膜增生引起的移植物衰竭需要精确了解控制每种不同类型的血流动力学调节机制。
All anastomotic intimal thickening may not be the same, and the underlying mechanism(s) regulating the different types may vary. We investigated the localization of experimental anastomotic intimal thickening in relation to known biomechanical and hemodynamic factors. Bilateral iliofemoral saphenous vein and polytetrafluoroethylene grafts were implanted in 13 mongrel dogs. The distal end-to-side anastomotic geometry was standardized, and the flow parameters were measured. After 8 weeks, seven of 10 animals (group 1) with patent grafts were killed and the anastomoses fixed by perfusion. Histologic sections from each anastomosis were studied with light microscopy; and regions of intimal thickening were identified and quantitated with use of oculomicrometry. To characterize the anastomotic flow patterns, transparent silicone models were constructed from castings of the distal anastomosis of three animals (group 11), and flow was visualized with use of helium-neon laser-illuminated particles under conditions simulating the in vivo pulsatile flow parameters. Histologic sections revealed two separate and distinct regions of anastomotic intimal thickening. The first, suture line intimal thickening, was greater in polytetrafluoroethylene anastomoses (0.35 +/- 0.23-mu-m) than in vein anastomoses (0. 15 +/- 0.03-mu-m, p < 0.05). The second distinct type of intimal thickening developed on the arterial floor and was the same in polytetrafluoroethylene (0.11 +/- 0.11-mu-m) and vein anastomoses (0.12 +/- 0.03-mu-m). Model flow visualization studies revealed a flow stagnation point along the arterial floor resulting in a region of low and oscillating shear where the second type of intimal thickening developed. High shear and short particle residence time were observed along the hood of the graft, an area devoid of intimal thickening. Regions of relatively low shear and long particle residence time formed along the lateral walls and heel of the anastomoses and were not specifically related to intimal thickening at the suture line. We conclude that at least two different types of anastomotic intimal thickening exist. Suture line intimal thickening represents vascular healing; greater prominence with prosthetic grafts may be related to compliance mismatch. Arterial floor intimal thickening is unrelated to graft type and develops in regions of flow oscillation and relatively low shear. In either situation the response is associated with altered flow conditions. Prevention of graft failure caused by occlusive intimal hyperplasia requires precise understanding of the hemodynamically modulated mechanisms that control each different type.