Complex Hemodynamic Insult in Combination with Wall Degeneration at the Apex of an Arterial Bifurcation Contributes to Generation of Nascent Aneurysms in a Canine Model
Complex Hemodynamic Insult in Combination with Wall Degeneration at the Apex of an Arterial Bifurcation Contributes to Generation of Nascent Aneurysms in a Canine Model
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复杂的血流动力学损伤与动脉分叉尖部的管壁变性相结合，导致犬模型中新生动脉瘤的产生
DOI：
10.3174/ajnr.a3926
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发表时间：
2014-09-01
影响因子：
3.5
通讯作者：
Cheng, Y. -S.
中科院分区：
文献类型：
--
作者：
Wang, J.;Tan, H. -Q.;Cheng, Y. -S.
背景和目的：脑动脉瘤产生的详细机制尚不清楚。我们的目的是研究特定的血流动力学损伤与动脉壁变性相结合是否会导致犬模型中动脉瘤的发生。材料和方法：在18只狗的颈总动脉中建立新的分支点。9只动物随后在动脉分叉尖端接受弹性蛋白酶损伤（弹性蛋白酶处理的分叉组）;对照分叉组（n = 9）接受生理盐水，3只犬的两条直颈总动脉接受弹性蛋白酶损伤（弹性蛋白酶处理的直颈总动脉组）。术后即刻、12周和24周进行血管造影和血流动力学分析;在12周和24周评价组织学反应。研究结果：血管造影显示，弹性蛋白酶处理分叉组5/9个模型的动脉分叉尖端存在新生动脉瘤（平均值为3.2 ± 0.4 mm）（对照分叉组和弹性蛋白酶处理直型组为0），未观察到任何动脉瘤破裂。组织学分析显示内弹性膜不连续，弹性纤维断裂，肌层变薄，平滑肌细胞增殖减少，炎性细胞增多，（巨噬细胞）浸润，弹性蛋白酶处理组中膜基质金属蛋白酶-2和基质金属蛋白酶-9的表达与对照组和弹性蛋白酶处理组相比有显著性差异（P <0.001）。术后血流动力学分析表明，在弹性蛋白酶处理的分叉组中，心尖经历了极低的壁切应力和流速以及最高的相对压力和总压力，而动脉壁重塑后这些值恢复正常。结论：在我们的研究中，在犬模型中，动脉分叉处的血流动力学损伤和动脉壁变性是产生动脉瘤所必需的。
BACKGROUND AND PURPOSE: The detailed mechanisms of cerebral aneurysm generation remain unclear. Our aim was to investigate whether specific hemodynamic insult in combination with arterial wall degeneration leads to the development of aneurysms in a canine model. MATERIALS AND METHODS: New branch points in the common carotid artery were created in 18 dogs. Nine animals subsequently received elastase insult at the arterial bifurcation apex (elastase-treated bifurcation group); the control bifurcation group (n = 9) received saline, and 3 dogs received an elastase insult to both straight common carotid arteries (elastase-treated straight group). Angiographic and hemodynamic analysis was performed immediately and 12 and 24 weeks' postsurgery; histologic response was evaluated at 12 and 24 weeks. RESULTS: Angiography revealed nascent aneurysms (mean, 3.2 ± 0.4 mm) at the arterial bifurcation apices in 5/9 models of the elastase-treated bifurcation group (versus 0 in the control bifurcation group and elastase-treated straight group) without any observed aneurysm rupture. Histologic analysis revealed internal elastic lamina discontinuity, elastic fiber disruption, a thinner muscular layer, reduced smooth-muscle cell proliferation, increased inflammatory cell (macrophage) infiltration, and expression of matrix metalloproteinase-2 and matrix metalloproteinase-9 in the media of the elastase-treated bifurcation group compared with that in either the control bifurcation group or the elastase-treated straight group (P < .001). Hemodynamic analysis after surgery indicated that the apex experienced extremely low wall shear stress and flow velocity and the highest relative and total pressure in the elastase-treated bifurcation group, while the values returned to normal after arterial wall remodelling. CONCLUSIONS: In our study, combined hemodynamic insult and arterial wall degeneration at arterial bifurcations are required for the generation of aneurysms in a canine model.