芎芍胶囊对兔实验性动脉粥样硬化血管重构的影响

目的 研究芎芍胶囊对实验性兔动脉粥样硬化(AS)模型血管重构的影响，并探讨其可能的机制。方法 采用4Fogarty导管剥脱损伤腹主动脉内皮后继喂高脂饲料的方法，复制兔节段性AS模型。术后随机分为8组，即模型3天组、2周组、6周组，单纯内皮损伤组，普罗布考组，芎芍胶囊小剂量组、大剂量组及正常对照组。除正常对照组及单纯内皮损伤组外均予高脂饲料喂养，对腹主动脉病变最明显处标本作病理形态学检查，并利用计算机图像分析系统观察动脉损伤后血管重构相关指标的变化及药物对其的影响并进行内膜增殖与血管重构的相关性分析。结果 球囊损伤腹主动脉内皮后，随时间延长，动脉内膜逐渐增厚，模型6周组与模型2周组及内皮损伤组比较差异有显著性(P<0．01)，芎芍胶囊大剂量与普罗布考组可明显减少内膜最大厚度(MIT)及内膜面积(IA)，与模型6周组比较差异有显著性(P<0．01)；随内膜增厚，动脉出现早期代偿性扩张，模型2周组内弹力膜围绕面积(IELa)、外弹力膜围绕面积(EELa)及管腔最小直径(MLD)、管腔面积(LA)均较正常组明显增加(P<0．01)，至模型6周时，随内膜进一步增厚，IELa、EELa反而有所缩小，血管代偿性扩张不足，管腔明显缩窄，MLD缩小(P<0．01)，各药物组均可增加MLD、LA，与模型6周组比较差异有显著性(P<0．01)。结论 单纯内皮损伤可能是病理性血管重构的始动因素之一，高脂血症可加重这一病理改变；内膜增殖和病理性血管重构共同参与了内皮损伤后AS管腔狭窄的病理过程；芎芍胶囊通过抑制球囊损伤后的内膜增殖，干预病理性血管重构，发挥防治AS作用。

Effect of Xiongshao Capsule on Vasc ular Remodeling in Rabbit with Experimental Atherosclerosis

OBJECTIVE: To study the effect of Xiongshao Capsule (XSC) on vascular remodeling in experimental atherosclerotic (AS) rabbits, and to explore the possible mechanisms. METHODS: Rabbit's fractional AS model was established by denuding and injuring the abdominal artery with 4F.Fogarty catheter, and followed with high cholesterol feeding. The animals were randomly divided into 8 groups, namely, the modeled group of 3 days, 2 weeks and 6 weeks after balloon injury (A, B and C); the single endothelium injury group (D), the probucol treating group (E), the low-dose and high-dose XSC treating group (F and G) and the normal control group (N). Except the rabbits in Group N and D, the other groups were all fed with high fat forage. Histopathological examination of abdominal aorta with the most obvious lesion was performed, and the changes of related vascular remodeling indexes after arterial injury were observed using computerized image analyzing system; the correlation analysis between progress of intimal proliferation and vascular remodeling were performed as well. RESULTS: Artery intimal proliferation progressed gradually as time went on, which was more significant in Group C as compared with that in Group B and D (P < 0.01). All the drugs could reduce the maximum intima thickness (MIT). Moreover, both high-dose XSC and Probucol profoundly decreased the intima area (IA), showing significant difference as compared with that in Group C (P < 0.01). The internal elastic laminal area (IELa), external elastic laminal area (EELa), minimum lumen diameter (MLD) and lumen area (LA) in Group A increased significantly, as compared with that in Group N (P < 0.01). At 6 weeks after balloon injury, with the further intimal thickening, IELa, EELa reduced contrarily, resulting in insufficient vascular compensation, lumen stricture and MLD reduction (P < 0.01). Improvement of MLD and LA was shown in all the drug treated groups, with significant difference in comparing with those in Group C (P < 0.01). CONCLUSION: Single endothelium injury may be one of the initiating elements of pathological vascular remodeling, which could be intensified by hyperlipemia. Intimal proliferation and vascular remodeling jointly participated in the pathological course of AS lumen stricture after endothelium injury. XSC plays its action in preventing and treating AS through inhibiting intimal proliferation after balloon injury and intervening pathological vascular remodeling.