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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、2 2d)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～ 2 2d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。
Objective To observe the main pathological changes of stenosis after vascular intimal injury and to study the changes of endothelin (ET) in plasma and endothelin (ET IR) in arterial tissues during the process of vascular intima injury. To investigate the relationship between vascular stenosis and ET changes in the relationship for the clinical treatment of ET for the treatment and prevention of restenosis after angioplasty to provide a theoretical basis. Methods Thirty rabbits were randomly divided into 6 groups according to different postoperative sacrificial time (6h, 1,3,7,15,22d), 5 in each group, 3 intima injury and 2 in control group (Sham). Preoperative and postoperative sacrifices were collected before the injection of micro-balloon catheter in the abdominal aorta animal model of endocardial injury. The control group was not inserted into the balloon catheter, radioimmunoassay was used to detect the level of ET in plasma, pathological morphology was used to observe the intima-media thickness and stenosis. The ET reaction in arterial tissue was detected by immunohistochemical method. Results The level of plasma ET in each group was significantly higher than that in the preoperative and postoperative groups, and the intimal thickening was found in the injured group. Vascular smooth muscle cells (VSMCs) proliferated and migrated to the internal elasticity The membrane layer, the accumulation of overlapping or even tumor-like protrusions caused by narrowing of the blood vessel, plasma ET levels and vascular intima-media thickness and stenosis was consistent. Conclusion VSMC proliferation and intimal thickening are the main pathological features of restenosis. ET is involved in cardiovascular contractions, VSMC proliferation and thrombosis and plays a key role in the process of vascular stenosis after balloon angioplasty. To antagonize or inhibit the biological effects of ET production may play an important clinical role in the prevention and treatment of restenosis.