Bosmans J M, Kockx M M, Vrints C J, Bult H, De Meyer G R, Herman A G
Department of Cardiology, University of Antwerp, Wilrijk, Belgium.
Arterioscler Thromb Vasc Biol. 1997 Apr;17(4):634-45. doi: 10.1161/01.atv.17.4.634.
The aim of the study was to assess the contribution of thrombus incorporation into neointimal thickening in the rabbit carotid artery after deep vascular injury induced by balloon angioplasty compared with superficial vascular injury induced by a perivascular collar. Besides CD 31 (PECAM 1), vimentin, alpha-smooth muscle actin, rabbit anti-macrophage monoclonal antibody and proliferating cell nuclear antigen, fibrin(ogen) and von Willebrand factor (vWF) deposition was assessed immunohistochemically. Angioplasty was performed in 47 rabbits and evaluated immediately (n = 7), after 6 hours (n = 4), and after 1 (n = 7), 2 (n = 9), or 3 (n = 20) weeks. A collar was placed in 29 rabbits and evaluated immediately (n = 5), after 6 hours (n = 5), and after 1 (n = 7), 2 (n = 10), or 3 (n = 2) weeks. After dilatation, the arteries were extensively denuded of endothelium, the internal elastic membrane was ruptured and blood-filled clefts were present in the media, pointing to deep vascular (type III) injury. Six hours later, mural fibrin(ogen) thrombi were formed, specially at sites with severe damage. This fibrin(ogen) matrix became infiltrated by phagocytes and smooth muscle cells. A luminal cap covered by regenerating endothelium was formed, demonstrating increased immunoreactivity to vWF. vWF was deposited in the extracellular neointimal spaces. Fibrin(ogen) thrombus deposition and incorporation appeared to be protracted phenomena for at least 2 weeks. After collar placement, minimal endothelial denudation was documented, pointing to focal superficial (type I) vascular injury. In subsequent weeks, neointimal thickening was associated with vWF deposition but not with fibrin(ogen) thrombus incorporation. In conclusion, mural fibrin(ogen) thrombus formation and incorporation contribute to neointima formation after deep vascular injury and seem to occur for several weeks after the initial insult.
本研究的目的是评估与血管周围套环诱导的浅表血管损伤相比，球囊血管成形术诱导的深部血管损伤后，兔颈动脉内血栓形成对新生内膜增厚的影响。除了CD 31（PECAM 1）、波形蛋白、α平滑肌肌动蛋白、兔抗巨噬细胞单克隆抗体和增殖细胞核抗原外，还采用免疫组织化学方法评估纤维蛋白（原）和血管性血友病因子（vWF）的沉积情况。对47只兔子进行血管成形术，并在术后即刻（n = 7）、6小时后（n = 4）、1周后（n = 7）、2周后（n = 9）或3周后（n = 20）进行评估。对29只兔子放置套环，并在术后即刻（n = 5）、6小时后（n = 5）、1周后（n = 7）、2周后（n = 10）或3周后（n = 2）进行评估。扩张后，动脉内皮广泛剥脱，内弹力膜破裂，中膜出现充满血液的裂隙，提示深部血管（III型）损伤。6小时后，形成了壁内纤维蛋白（原）血栓，特别是在损伤严重的部位。这种纤维蛋白（原）基质被吞噬细胞和平滑肌细胞浸润。形成了由再生内皮覆盖的管腔帽，显示对vWF的免疫反应性增加。vWF沉积在细胞外新生内膜间隙中。纤维蛋白（原）血栓的沉积和形成似乎是至少持续2周的过程。放置套环后，记录到最小程度的内皮剥脱，提示局灶性浅表（I型）血管损伤。在随后的几周内，新生内膜增厚与vWF沉积有关，但与纤维蛋白（原）血栓形成无关。总之，壁内纤维蛋白（原）血栓的形成和形成对深部血管损伤后的新生内膜形成有贡献，并且似乎在初始损伤后数周内发生。
