The examination of neointimal hyperplasia in injured animal artery models has furthered our understanding of angioplasty and stenting mechanisms . In the majority of models, an injurious stimulus is directly inflicted upon the normal, intact artery to facilitate intimal thickening. Intravascular techniques include endothelial cell denudation by the passage of a balloon embolectomy catheter, the distension of the artery by balloon angioplasty, implantation of a stent and desiccation by blowing a stream of air through the lumen. These strategies may mimic the cellular processes that characterize the 'response to injury' restenosis following percutaneous, catheter-mediated interventions in patients . They also incur a degree of damage to the vessel wall media, disrupt the internal elastic lamina and may induce the complications that are also encountered in the clinical setting such as thrombosis, dissection and rarely, wall rupture. Perivascular techniques, which directly damage the native endothelium, are also employed such as electrical stimulation and application of a rigid (polyethylene) collar. The periadventitial placement of a biologically inert, flexible silicone collar (or cuff) around the common carotid artery in the rabbit has also been extensively used . This strategy involves minimal trauma to the vessel wall and generates a neointima that leaves the endothelium intact. Since endothelial dysfunction is a key pathological process that underlies occlusive vascular pathology, the contributory impact of the preserved endothelium can also be controlled for and assessed in this model. Variations of the cuff approach to induce neointimal formation have successfully been extended to the rat, mouse  and porcine carotid arteries and mouse femoral artery.
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