去势对雄性大鼠血管成形术后再狭窄的影响

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。

Effect of Castration on Restenosis after Precutanous Transluminal Angioplasty in Male Rats

OBJECTIVE: To observe the developing changes of adventitia in restenosis after precutaneous transluminal angioplasty(PTA), and investigate the effect of androgen on restenosis through contrasting the castrated male rat models and its mechanism. METHODS: Models were constructed of castrated male rats and restenosis of the common carotid artery, and specimens were collected at the 3rd, 7th, 14th and 28th day respectively after modeling. Hematoxylin and eosin staining, immunohistochemical staining, and electronic microscopy were performed to observe the condition of restenosis. RESULTS: Proliferating cells occurred in adventitia first and phenotype of adventitial cells was changed at the 3rd day after PTA. The adventitial proliferating index was the highest at the 7th day after PTA, and proliferating migration towards intimal was observed. The proliferating cells mostly occurred in the middle layer and neointima at the 14th day after PTA. The areas of adventitia and neointima were larger and the degrees of restenosis were higher in the castrated rats than in the non-castrated ones at different time points. Take the 14 d group, the adventitial area was[(3,566 +/- 337) micron2 vs (2,751 +/- 401) micron2, P = 0.008], the neointimal area[(3,553 +/- 477) micron2 vs (2,757 +/- 435) micron2, P = 0.025], the restenosis rate[(76 +/- 2)% vs (60 +/- 8)%, P = 0.005], and the proliferating index [(29 +/- 2)% vs (13 +/- 1)%, P < 0.001]. CONCLUSION: Adventitial proliferation and migration contribute to restenosis after PTA; Androgen in rats can physiologically relieve restenosis, probably through intervening in the activation of adventitia.