兔腹主动脉球囊成形术后狭窄过程中内皮素的动态变化

目的观察血管内膜损伤后狭窄过程的主要病理变化特征，研究此过程中血浆内血管内皮素(ET)水平及局部动脉组织内ET反应性(ET-IR)的改变，以探讨血管狭窄的发生与ET变化的关系。为临床寻求针对ET因素的治疗处理和预防血管成形术后再狭窄提供理论依据。方法大耳白兔30只，依术后处死时间不同(6h和1、3、7、15、22d)随机分为6组，每组5只，3只内膜损伤、2只组内对照(假手术)。术前及术后处死前均采血，置入微球囊导管于腹主动脉内拉动制备内膜损伤动物模型。对照组不插入球囊导管，以放射免疫法检测血浆内ET水平，行病理形态学观察血管内膜厚度及管腔狭窄情况，以免疫组织化学法检测动脉组织内ET反应。结果损伤组各时间段血浆ET水平均较术前及假手术组有明显升高，损伤组血管内膜增厚，术后15～22d时可见血管平滑肌细胞(VSMC)增殖并迁移到内弹力膜层内，堆积重叠甚至呈瘤样突起而致血管腔变窄，血浆ET水平与血管内膜厚度及管腔狭窄程度呈一致性。结论VSMC增殖和内膜增厚是再狭窄的主要病理特征。ET参与心血管收缩、VSMC增殖和血栓形成，在血管球囊成形术后血管狭窄过程中起到了关键的作用。拮抗或抑制ET生成的生物学作用，对防治再狭窄可能具有重要的临床意义。

Study on the dynamic change of endothelin in the development of stenosis of aorta after balloon injury in rabbits

Objective To study the dynamic change of endothelin (ET) in the blood with pathological and immunohistochemical changes of ET(ET-immunoreaction, ET-IR) in the development of stenosis of rabbit aorta after transluminal angioplasty.Methods According to the different periods of being killed after micro-balloon angioplasty, 30 rabbits were divided randomly into 6 groups including 6-hour group, 1-day group, 3-day group, 7-day group, 15-day group and 22-day group. 3 out of 5 rabbits in each group were created as models of aortic endothelium injury by micro-balloon angioplasty, the rest 2 rabbits were taken as control. ET levels in the plasma were measured by ELISA before, as well as after micro-balloon angioplasty. Pathomorphological examination of the local traumatic aorta was carried out to observe the intimal thickness and the extent of lumen stenosis, and ET-IR was assessed by immunohistochemical technique performed on aortic wall after micro-balloon angioplasty. Results (1) The major change of vascular stenosis was proliferation of vascular smooth muscle cell (VSMC) and endothelium. (2) ET levels in the plasma and ET-IR on the local aortic wall were significantly increased after micro-balloon angioplasty.Conclusions The experimental results show that the major pathologic change of vascular stenosis is the obvionus proliferation of VSMC and endothelium. Further more, ET is a key factor in the development of vascular stenosis.