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目的观察兔髂动脉再狭窄模型病理改变,并加用替米沙坦进行干预,探讨其对再狭窄模型新生内膜增殖的影响。方法 30只新西兰大白兔随机分为对照、再狭窄和替米沙坦组,每组10只。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,其中替米沙坦组于第二次球囊损伤后第2天开始加用替米沙坦5mg/(kg·d)。实验结束时,动物处死前采血检测总胆固醇,并留取髂动脉标本,行苏木精伊红染色法染色及免疫组化检测,组织匀浆测定血管紧张素Ⅱ(AngⅡ)水平。结果与对照组比较,再狭窄和替米沙坦组总胆固醇[(20.44±0.68)、(20.39±0.60)比(0.58±0.19)mmol/L]、血管壁AngⅡ[(115.6±15.7)、(123.8±22.1)比(90.1±7.7)ng/L]、内膜厚度[(266.1±70.3)、(68.2±24.4)比(2.8±0.2)μm]和狭窄率[(89.3±6.9)%、(42.6±18.1)%比(23.0±3.5)%]增加(均P<0.05)。而替米沙坦组的内膜厚度和狭窄率低于再狭窄组(均P<0.01)。与对照和替米沙坦组比较,再狭窄组平滑肌细胞增殖率明显增加[(21.9±4.7)%比(7.3±4.9)%、(7.1±5.1)%,均P<0.01]。α平滑肌肌动蛋白染色证实,再狭窄和替米沙坦组的新生内膜主要细胞成分为血管平滑肌细胞。结论替米沙坦对兔髂动脉再狭窄模型血管平滑肌细胞增殖及新生内膜增殖均有抑制作用。
Objective To observe the pathological changes of the rabbit iliac artery stenosis model and add Telmisartan to interfere the neointimal hyperplasia in the model of restenosis. Methods Thirty New Zealand white rabbits were randomly divided into control group, restenosis group and telmisartan group, with 10 rats in each group. The model of restenosis was established by feeding high-fat diet combined with iliac artery secondary balloon injury. The telmisartan group was treated with telmisartan 5mg / (kg · d) on the second day after the second balloon injury. . At the end of the experiment, animals were sacrificed and blood samples were collected for determination of total cholesterol. Samples of iliac arteries were collected and stained with hematoxylin and eosin staining and immunohistochemistry. Tissue homogenate was used to measure the level of angiotensin Ⅱ (AngⅡ). Results Compared with the control group, the levels of total cholesterol ([(20.44 ± 0.68) vs (20.39 ± 0.60) vs (0.58 ± 0.19) mmol / L], AngⅡ [(115.6 ± 15.7) 123.8 ± 22.1 vs 90.1 ± 7.7 ng / L], the thickness of intima [(266.1 ± 70.3) vs (68 ± 24.4) vs (2.8 ± 0.2) μm] and the stenosis rate (89.3 ± 6.9% 42.6 ± 18.1)% (23.0 ± 3.5)%] (all P <0.05). Intima thickness and stenosis rate were lower in the telmisartan group than in the restenosis group (all P <0.01). Compared with the control group and the telmisartan group, the proliferation rate of smooth muscle cells in restenosis group was significantly increased (21.9 ± 4.7% vs 7.3 ± 4.9%, 7.1 ± 5.1%, both P <0.01). α-smooth muscle actin staining confirmed that the main neoplastic components of restenosis and telmisartan were vascular smooth muscle cells. Conclusion Telmisartan can inhibit the proliferation of vascular smooth muscle cells and neointimal hyperplasia in rabbit model of iliac artery stenosis.