目的:通过建立兔髂动脉再狭窄模型,观察髂动脉病理改变及连接蛋白(Cx)的表达情况。方法:20只新西兰大白兔随机分为对照组与再狭窄组,采用高脂饲料喂养联合兔髂动脉二次球囊损伤建立再狭窄模型。所有髂动脉标本均行HE染色及免疫组织化学检测,采用RT-PCR法测定血管组织匀浆Cx43及Cx40mRNA表达。结果:与对照组相比,再狭窄组髂动脉管腔狭窄率增大[(23.00±3.53)%︰(89.32±6.93)%,P<0.01],内膜明显增厚[(266.12±70.27)μm︰(2.85±0.19)μm,P<0.01],α-平滑肌肌动蛋白(α-SMA)染色证实新生内膜主要细胞成分为血管平滑肌细胞(VSMCs)。免疫组织化学结果显示,两组均有Cx43表达,再狭窄组新生内膜处有大量Cx43表达,较正常对照组明显增强。两组血管ECs及中膜均有Cx40表达,再狭窄组Cx40表达仅比对照组略有增强。RT-PCR结果显示,与正常对照组比较,再狭窄组Cx43mRNA表达增加(P<0.01);但两组Cx40mRNA表达量差异无统计学意义。结论:新生内膜增殖是再狭窄的病理基础,VSMCs是主要的增殖细胞成分,并且这一过程伴随有Cx43的表达增加,而Cx40表达无变化。 Objective: To establish a rabbit model of iliac artery restenosis and observe the pathological changes of iliac artery and the expression of connexin (Cx). Methods: Twenty New Zealand white rabbits were randomly divided into control group and restenosis group. The model of restenosis was established by feeding high fat diet combined with iliac artery secondary balloon injury. All iliac arteries were examined by HE staining and immunohistochemistry. The expression of Cx43 and Cx40 mRNA in vascular homogenate was determined by RT-PCR. Results: Compared with the control group, the stenosis rate of iliac artery in restenosis group was significantly higher than that in control group [(23.00 ± 3.53)% vs (89.32 ± 6.93)%, P <0.01], and significantly thicker intima [(266.12 ± 70.27) (2.85 ± 0.19) μm, P <0.01]. The main components of neointimal formation were vascular smooth muscle cells (VSMCs), which were confirmed by α-smooth muscle actin (α-SMA) staining. Immunohistochemical results showed that Cx43 expression was found in both groups, and there was a large number of Cx43 expression in the neointima of the restenosis group, which was significantly higher than that of the normal control group. The expression of Cx40 in vascular ECs and medial membranes of both groups was only increased slightly in the restenosis group compared with the control group. The results of RT-PCR showed that the expression of Cx43 mRNA in restenosis group was increased compared with that in normal control group (P <0.01). However, the expression of Cx40 mRNA in two groups had no significant difference. CONCLUSION: Neointimal hyperplasia is the pathological basis of restenosis. VSMCs are the major proliferating cell components, accompanied by an increase of Cx43 expression and no change of Cx40 expression.