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目的:制作小型猪冠状动脉炎症型支架再狭窄模型,用定量冠状动脉造影、测定支架处血管壁内膜增生程度及炎症因子表达等方法探讨雷帕霉素及紫杉醇涂层支架对炎症性冠状动脉狭窄的抑制作用。方法:小型雄性家猪14头,开胸法将冠状动脉外膜包裹吸附白介素-1β(IL-1β)琼脂糖微粒悬液的纸巾。2周后,用定量冠状动脉造影观察管腔狭窄程度及随机分为雷帕霉素支架组(n=7)、紫杉醇支架组(n=9)及裸支架组(n=8)。1个月后进行随访定量冠状动脉造影测定各组冠状动脉支架节段内和支架内的最小管腔直径(MDL),参照管腔直径(RLD),管腔狭窄百分比(DS),计算出晚期管腔丢失(LLL)进行对比分析。塑料包埋法进行支架血管切片,测定管腔增生面积及血管壁单核细胞趋化因子-1(MCP-1)、肿瘤坏死因子-α(TNF-α)、P-选择素、血管细胞间黏附因子-1(VCAM-1)的表达。结果:冠状动脉外膜包裹IL-1β血管段局限性狭窄平均达到70％以上。裸支架组中冠状动脉支架节段内和支架内的LLL明显高于雷帕霉素支架组和紫杉醇支架组,且再狭窄(DS)率高。雷帕霉素支架组及紫杉醇支架组冠状动脉支架节段内和支架内LLL均低于裸支架组,且明显抑制内膜增生(P<0．01)。但只有雷帕霉素支架组明显下调MCP-1,TNF-α,P-选择素和VCAM-1的表达。结论:雷帕霉素和紫杉醇药物洗脱支架对IL-1β诱发的小型猪冠状动脉炎症性狭窄均有较好的抗内膜增殖作用,但在LLL指标及抑制内膜增生方面雷帕霉素优于紫杉醇药物洗脱支架,有可能是通过直接或间接抗炎机制达到的。
OBJECTIVE: To make mini-swine coronary artery stenosis model with coronary artery stenosis, to evaluate the effect of rapamycin and paclitaxel-coated scaffold on inflammatory coronary arteries by quantitative coronary angiography, intimal hyperplasia and expression of inflammatory cytokines in scaffolds. Narrow inhibition. Methods: A total of 14 small male domestic pigs were enrolled in this study. The thoracotomy was performed by wrapping the coronary adventitial membrane with a tissue suspension containing interleukin-1β (IL-1β) agarose particles. Two weeks later, the degree of stenosis was observed by quantitative coronary angiography and was randomly divided into rapamycin group (n = 7), paclitaxel group (n = 9) and bare stent group (n = 8). One month later, follow-up quantitative coronary angiography was performed to determine the minimum lumen diameter (MDL), the reference lumen diameter (RLD) and the lumen stenosis percentage (DS) Lumen loss (LLL) for comparative analysis. Plastic embedding method was used for vascular scaffold. The area of luminal hyperplasia and the expression of MCP-1, TNF-α, P-selectin, Expression of adhesion molecule-1 (VCAM-1). Results: The limitation of stenosis of IL-1β in coronary artery was more than 70%. The LLL was significantly higher in the bare stent group than in the rapamycin stent group and the paclitaxel stent group, and the rate of restenosis (DS) was higher in the coronary stent segment and in the stent. LLL in rapamycin-eluting stent and paclitaxel-treated stent group were lower than those in bare stent group, and significantly inhibited intimal hyperplasia (P <0.01). However, only rapamycin scaffold significantly downregulated the expression of MCP-1, TNF-α, P-selectin and VCAM-1. Conclusion: Both rapamycin and paclitaxel-eluting stent have a good anti-intimal proliferation effect on IL-1β-induced miniature porcine coronary artery stenosis. However, in terms of LLL index and inhibition of intimal hyperplasia, rapamycin Outperforming paclitaxel-eluting stents, it is possible to achieve this through direct or indirect anti-inflammatory mechanisms.