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目的 :系统观察血管外膜细胞在血管成形术 (PTA)后再狭窄过程中的动态变化 ,通过复制去势模型对照观察雄激素对再狭窄的影响 ,并探讨其作用机制。 方法 :复制雄性SD大鼠的去势模型及颈总动脉再狭窄模型 ,于术后 3、7、14、2 8d不同时间点取材 ,行苏木精 伊红染色及免疫组化染色 ,并以电镜观察血管狭窄情况。 结果 :PTA术后 3d增殖细胞首先出现在血管外膜 ,并发生表型转变 ,术后 7d时外膜细胞增殖最明显 ,并向内膜迁移 ,术后 14d外膜细胞增殖减少 ,增殖细胞集中于中膜及新生内膜。各观察时间点 ,去势雄性大鼠的血管外膜面积、新生内膜面积、血管狭窄程度 ,均较未去势组大。以 14d组为例 ,血管外膜面积 [(35 6 6± 337) μm2 vs (2 75 1± 4 0 1) μm2 ,P =0 .0 0 8],新生内膜面积 [(35 5 3± 4 77) μm2 vs (2 75 7± 4 35 ) μm2 ,P =0 .0 2 5 ],血管狭窄程度 [(76± 2 ) %vs (6 0±8) % ,P =0 .0 0 5 ],外膜细胞增殖指数 [(2 9± 2 ) %vs (13± 1) % ,P <0 .0 0 1]。 结论 :PTA术后血管外膜细胞增殖、迁移参与了再狭窄的形成。生理状态下体内雄激素可以减轻血管再狭窄程度 ,其作用机制可能与干预血管外膜细胞活化有关。
OBJECTIVE: To systematically observe the dynamic changes of vascular adventitial cells during restenosis after angioplasty (PTA), and to observe the effect of androgens on restenosis by replicating ovariectomy model and to explore its mechanism. Methods: The model of castration and common carotid artery restenosis in male Sprague-Dawley rats were duplicated. The rats were drawn at 3, 7, 14 and 28 days after operation. The hematoxylin and eosin staining and immunohistochemistry Electron microscopy of vascular stenosis. RESULTS: On the 3rd day after PTA, proliferating cells first appeared on the adventitia and showed phenotypic changes. At 7 days after operation, the adventitial cells proliferated most obviously and migrated to the intima. At the 14th day after operation, the adventitial cells proliferated and the proliferating cells were concentrated In the membrane and neointima. At each observation time point, the area of adventitia, the area of neointimal area and the degree of stenosis of castrated male rats were larger than those of the untreated group. Taking 14d group as an example, the area of adventitial membrane was (35 6 6 ± 337) μm 2 vs (2 75 1 ± 4 0 1) μm 2, P 0 0 0 8] 4 77) μm 2 vs (75 75 ± 4 35) μm 2, P 0. 05 2 5, and the degree of vascular stenosis [(76 ± 2)% vs (60 ± 8)%, P = ], Adventitial cell proliferation index [(29 ± 2)% vs (13 ± 1)%, P <0.01]. Conclusion: The proliferation and migration of vascular adventitial cells after PTA are involved in the formation of restenosis. Androgen in vivo can reduce the degree of vascular restenosis, and its mechanism may be related to the activation of vascular adventitial cells.