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A novel model of accelerated intimal hyperplasia in the pig iliac artery

机译:猪动脉内膜增生的新模型

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摘要

There is no good animal model of large artery injury-induced intimal hyperplasia (IH). Those available are reproducible, providing only a few layers of proliferating cells or have the disadvantage of the presence of a metallic stent that complicates histology evaluation. This study was designed to develop a new, simple model of accelerated IH based on balloon injury in conjunction with disruption of the Internal Elastic Lamina (IEL) in pig external iliac arteries. Iliac artery injury (n = 24) was performed in 12 Yorkshire pigs divided in two groups: Group I (n = 10), overdistention injury induced by an oversized non-compliant balloon; Group II (n = 14), arterial wall disruption by pulling back an isometric cutting balloon (CB) followed by stretching with a compliant Fogarty Balloon (FB). At two weeks, arteries were processed for morphometric analysis and immunohistochemistry (IHC) for smooth muscle cells (SMC) and proliferating cell nuclear antigen (PCNA). When comparing the two groups, at 2 weeks, arteries of group II had a higher incidence of IH (100%vs. 50%, P = 0.0059), increased intimal areas (2.54 ± 0.33 mm2vs. 0.93 ± 0.36 mm2, P = 0.004), increased intimal area/Media area ratios (0.95 ± 0.1 vs. 0.28 ± 0.05; P<0.0001) and decreased lumen areas (6.24 ± 0.44 vs. 9.48 ± 1.56, P=0.026). No thrombosis was noticed in Group II. Neointima was composed by proliferating SMC located with the highest concentration in the area of IEL disruption (IHC). Arterial injury by pulling back CB and FB induces significant IH in pig iliac arteries by two weeks without thrombosis. This model is superior to the classical overdistention non-compliant model and should be useful and cost-effective for preclinical testing of procedures designed to inhibit IH in large peripheral arteries.
机译:没有大动脉损伤引起的内膜增生(IH)的良好动物模型。可用的那些是可复制的,仅提供几层增殖细胞,或具有​​金属支架的缺点,这会使组织学评估复杂化。这项研究旨在开发一种新的,简单的,基于球囊损伤并破坏猪external外动脉内弹力层(IEL)的IH加速模型。 12动脉损伤(n = 24)在12只约克郡猪中进行,分为两组:I组(n = 10),由过大的不顺应性气球引起的过度扩张损伤;第II组(n = 14),通过向后拉等距切割球囊(CB),然后用顺应性Fogarty球囊(FB)拉伸来破坏动脉壁。在两周时,对动脉进行平滑肌细胞(SMC)和增殖性细胞核抗原(PCNA)的形态分析和免疫组化(IHC)。比较两组,在第2周时,第二组的动脉IH发生率更高(100%vs. 50%,P = 0.0059),内膜面积增加(2.54±0.33 mm 2 vs 0.93±0.36 mm 2 ,P = 0.004),内膜面积/介质面积比增加(0.95±0.1 vs. 0.28±0.05; P <0.0001),内腔面积减少(6.24±0.44 vs.)。 9.48±1.56,P = 0.026)。在第二组中未发现血栓形成。新内膜是由IEL破坏(IHC)区域中浓度最高的SMC增殖所组成。撤回CB和FB引起的动脉损伤可在两周内在猪动脉中诱导明显的IH,而无血栓形成。该模型优于经典的过度扩张非顺应性模型,并且在临床前测试旨在抑制大型外周动脉中的IH的程序中应该是有用且具有成本效益的。

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