茶多酚对兔颈总动脉血管成形术后再狭窄的影响

为探讨茶多酚对血管成形术后动脉中膜平滑肌增生及胶原增生的影响,以及与组织型纤溶酶原激活物和血管紧张素Ⅱ活性改变的关系,将雄性新西兰白兔30只随机分为对照组、低剂量茶多酚组和高剂量茶多酚组,用球囊导管剥脱右颈总动脉内皮,造成内皮及中膜损伤,分别在术前、术后3、7、11、14、22和28 d采动脉血应用酶联免疫法测血浆组织型纤溶酶原激活物活性及放射免疫法测血管紧张素Ⅱ血清水平,术后28 d处死动物并取右颈总动脉观察动脉中膜平滑肌和胶原增生程度.结果发现,高剂量茶多酚组组织型纤溶酶原激活物血浆活性为0.169±0.067 IU/L,低剂量茶多酚组为0.141±0.043 IU/L,对照组为0.126±0.043 IU/L,高剂量茶多酚组高于对照组和低剂量茶多酚组,差异具有显著性(P<0.05).高剂量茶多酚组血管紧张素Ⅱ血清水平为1 229±283 ng/L,低剂量茶多酚组为1 302±284 ng/L,对照组为1 309±263 ng/L,三组动物术后血管紧张素Ⅱ血清水平比较差异无显著性.高剂量茶多酚组动脉中膜胶原含量为50.1%+5.82%、低剂量茶多酚组为56.7%±2.3%,对照组为62.8%±2.1%,高剂量茶多酚组低于对照组及低剂量茶多酚组,差异具有显著性 (P<0.05);低剂量茶多酚组低于对照组,差异具有显著性(P<0.001).高剂量茶多酚组中膜平滑肌细胞计数为0.022±0.006/μm2,低剂量茶多酚组为0.034±0.008/μm2,对照组为0.033±0.007/μm2,高剂量茶多酚组低于对照组及低剂量茶多酚组,差异具有显著性(P<0.01).结果提示,高剂量茶多酚可提高血管成形术后血浆组织型纤溶酶原激活物活性,对血管紧张素Ⅱ血清水平无显著性影响,可抑制动脉中膜胶原及平滑肌细胞的增生,这可能有助于减轻或预防动脉血管成形术后再狭窄.

Adventitial Inflammation Induces the Formation and Progress of the Atherosclerotic Lesions within Coronary Artery of ApoE Knockout Mice

Aim To observe the occurrence and the morphological manifestation of atherosclerotic lesions in apolipoprotein E gene knockout (ApoE -/-) mice. Explore the relationship between lesion formation and adventitial inflammation. Methods The successive sections of the hearts of 60 and 112 weeks old ApoE -/- mice were made, then stained by Movat method. Trailled all the trunks and intra-myocardial small branches of coronary arteries for finding the lesions, and analyzed the relationship between lesion distribution and adventitial inflammation. The aseptic adventitial inflammation of the femoral artery in C57BL/6 mice were duplicated, detected the expression of adhesive molecules. Results There were extending lesions in the trunks of coronary artery, which extended directly from the aorta. There were in situ lesions in the branches of the trunks (including intra-myocardial small branches). There were inflammatory cells aggregation at the adventitia with the lesions at the corresponding intima. The infiltrating area of inflammatory cells was much larger than the area of lesion at intima. Some positions with inflammatory infiltration in adventitia could be seen without lesion at corresponding intima. All the in situ lesions were arised within ventricular muscle, most of the large in situ lesions appeared in the left ventricular wall. ICAM-1, VCAM-1 and adhesion of white blood cells could be seen at the intima of femoral artery in the mice with experimental aseptic adventitial inflammation. Conclusions The adventitial inflammation is one of the predisposing factors for the formation of lesions within the coronary artery.