血管球囊损伤后内膜增生及血管重塑对再狭窄的影响

目的:探讨在血管再狭窄形成过程中内膜增生及血管重塑的作用.方法:采用大鼠颈动脉球囊损伤后血管再狭窄的动物模型,经形态学观察及计算机图像分析,观测术后不同时间点血管壁各成分的变化. 结果:血管损伤后3 d血管内腔面可见增殖的血管平滑肌细胞,损伤后7 d新生内膜形成并继续增厚,损伤后28 d新生内膜厚度及面积达最大,损伤后35 d较损伤后28 d缩小(P<0.01). 损伤后各时间点中膜厚度无明显变化,但损伤后35 d的中膜面积较损伤后28 d及对照未损伤侧缩小(P<0.05). 管腔面积于损伤后前3 d略增大,损伤后7 d出现管腔面积减少,至损伤后28~35 d管腔面积明显小于对照未损伤侧(P<0.01). 外弹力膜内横截面积在损伤后3~7 d略增大,损伤后14 d最大,损伤后35 d较损伤后28 d及对照未损伤侧明显缩小(P<0.01). 结论:内膜增生与血管重塑是再狭窄形成的主要病理机制,血管再狭窄的形成是内膜增生与血管重塑的平衡所决定的,两者共同导致管腔狭窄.

Effects of intimal hyperplasia and vascular remodeling on vascular restenosis after balloon injury

AIM: To explore the role of intimal hyperplasia and vascular remodeling in the formation of vascular restenosis. METHODS: The model of vascular restenosis established by balloon injury of rat carotid arteries was used and pathologic changes of the arterial wall at different times after balloon injury were observed by microscopy and computer image analyzing system. RESULTS: The proliferation of vascular smooth muscle cell (VSMC) was spotted on the surface of vascular lumen at 3 d after balloon injury, and at 7 d after injury, the neointima formed and continuously thickened. At 28 d after injury, the thickness and the area of the neointima reached their maximal, but at 35 d after injury, they were smaller than those at 28 d after injury. The thickness of the media at different times after balloon injury had no significant change, but the area of the media at 35 d after injury was smaller than that at 28 d after injury, and the area in injured vessels was smaller than that in non injured vessels. The lumen area slightly increased at 3 d after injury and decreased at 7 d after injury. At 28 to 35 d after injury, the lumen area obviously decreased, compared with the non injured control vessels. The cross sectional area bounded by the external elastic lamina slightly increased at 3 to 7 d after injury, reaching maximal at 14 d after injury, but at 35 d after injury it was significantly smaller than that at 28 d after injury and that of non injured control vessels. CONCLUSION: Intimal hyperplasia and vascular remodeling are important pathological factors in the pathogenesis of vascular restenosis. The balance of intimal hyperplasia and vascular remodeling are responsible for the formation of vascular restenosis and they together result in lumen narrowing.