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目的:观察氯吡格雷对兔髂腹动脉球囊损伤后血管内皮功能及平滑肌细胞的影响。方法:37只新西兰兔随机分为正常组(n=7)、模型组(n=10)、氯吡格雷组(n=10)和阿托伐他汀组(n=10)。后3组通过高胆固醇喂养加髂动脉内膜剥脱建立动脉硬化模型。用生物化学技术检测血管成形术前后血清内皮素、一氧化氮浓度;用光镜、扫描电镜、透射电镜观察髂动脉损伤术后8周血管病理形态学改变并测量动脉内膜、中膜厚度和面积;用原位杂交技术检测血小板源性生长因子(PDGFmRNA)的表达。结果:①与模型组相比,氯吡格雷组和阿托伐他汀组血清内皮素浓度均降低,一氧化氮浓度均升高,差异有统计学意义(P<0.05,P<0.01);②氯吡格雷组和阿托伐他汀组动脉内膜厚度与内膜/中膜厚度比显著减少(P<0.05),内膜面积与内膜/中膜面积比明显减少(P<0.05);③PDGFmRNA的表达明显降低(P<0.05);④透射电镜见模型组血管损伤段平滑肌细胞胞体肥大,核增大,胞浆内线粒体、粗面内质网增加,胞内吞噬大量脂滴,呈“合成型”改变。氯吡格雷组和阿托伐他汀组增生的平滑肌细胞胞体及核较小,胞浆内粗面内质网、线粒体较少,胞内吞噬的脂滴较少,接近“收缩型”改变。扫描电镜示模型组内皮细胞排列紊乱,细胞连接破坏,有大量血小板和蛋白颗粒粘附;氯吡格雷组和阿托伐他汀组内皮细胞排列趋于正常,细胞连接恢复,血小板粘附少。结论:氯吡格雷能保护血管内皮功能,减轻球囊损伤后PDGF表达,抑制平滑肌细胞增殖和血管内膜增生,预防动脉粥样硬化的形成和发展。
OBJECTIVE: To observe the effect of clopidogrel on vascular endothelial function and smooth muscle cells after balloon injury in ilio-abdominal artery in rabbits. Methods: 37 New Zealand white rabbits were randomly divided into normal group (n = 7), model group (n = 10), clopidogrel group (n = 10) and atorvastatin group (n = 10). The latter three groups were given arteriosclerosis model by hypercholesterolemic feeding and iliac artery dissection. The levels of endothelin and nitric oxide in serum before and after angioplasty were detected by biochemical techniques. The pathological changes of blood vessels were observed 8 weeks after the iliac artery injury with light microscope, scanning electron microscope and transmission electron microscope. The intima and media thickness And area; using in situ hybridization detection of platelet-derived growth factor (PDGFmRNA) expression. Results: ① Compared with model group, serum endothelin concentration and concentration of nitric oxide in both clopidogrel group and atorvastatin group were significantly increased (P <0.05, P <0.01); ② The ratio of intima-media thickness to intima-media thickness was significantly decreased in clopidogrel and atorvastatin groups (P <0.05), and the ratio of intima-media area to intima / media area was significantly decreased (P <0.05) (P <0.05). (4) Transmission electron microscopy showed that the vascular smooth muscle cells in the vascular injury group were hypertrophy, nuclear enlargement, increased mitochondria and rough endoplasmic reticulum in the cytoplasm, Type “change. Clopidogrel group and atorvastatin group proliferated small smooth muscle cell bodies and nuclei, rough endoplasmic reticulum cytoplasm, less mitochondria, intracellular phagocytosed lipid droplets less, close to the ”shrinkage" changes. Scanning electron microscopy showed that endothelial cells were disordered, cell junctions were disrupted, and a large number of platelets and protein granules adhered. In the clopidogrel group and atorvastatin group, the endothelial cells tended to be normal and the cell connections recovered with less platelet adhesion. Conclusion: Clopidogrel can protect vascular endothelial function, reduce the expression of PDGF after balloon injury, inhibit the proliferation of smooth muscle cells and intimal hyperplasia, prevent the formation and development of atherosclerosis.