Wilensky R L, March K L, Gradus-Pizlo I, Sandusky G, Fineberg N, Hathaway D R
Krannert Institute of Cardiology, Department of Medicine, Roudebush VA Medical Center, Indiana University School of Medicine, Indianapolis, 46202-4800, USA.
Circulation. 1995 Nov 15;92(10):2995-3005. doi: 10.1161/01.cir.92.10.2995.
Several nonatherosclerotic animal models of restenosis exist and are used for the evaluation of the vascular response to angioplasty-induced injury. However, few studies have evaluated the response of an atherosclerotic vessel to angioplasty. The present study examined the radiographic, histological, immunohistochemical, and morphometric responses over time of atherosclerotic rabbit femoral arteries after percutaneous transluminal angioplasty (PTA).
Rabbits (n = 94) underwent arterial dissection and were fed a hypercholesterolemic diet for 3 weeks, and then PTA was performed. Arteries were obtained before PTA and 1, 3, 5, 7, 14, and 28 days after PTA. PTA caused radial stretching of the artery, medial compression, intramural hemorrhage, injury to normal arterial segments, and dissection within the intima and media. Thrombus filled and cellular accumulation repaired the dissection. Peak smooth muscle cell and macrophage DNA synthesis was noted at 3 to 5 days after angioplasty, generally at the dissection but also in normal sections of the artery. Adventitial injury and subsequent adventitial cellular proliferation and collagen production were observed. A rapid decrease in the radiographic minimal luminal diameter was noted at 3 days, resulting from vascular recoil or thrombus filling the dissection. At 7 to 14 days, only 24% to 33% of the luminal loss was accounted for by an increase in the intimal area, and 22% to 28% of the intima was neointima.
Restenosis in an atherosclerotic artery results from a variable combination of intimal proliferation, vascular remodeling/wound contraction, and recoil of the normal section of the artery. The variability of an atherosclerotic artery to PTA injury results from variable dissection, thrombus formation, and cellular response to injury as well as variable scar contraction and elastic recoil.
存在几种非动脉粥样硬化性再狭窄动物模型，并用于评估血管对血管成形术所致损伤的反应。然而，很少有研究评估动脉粥样硬化血管对血管成形术的反应。本研究检测了经皮腔内血管成形术（PTA）后兔股动脉粥样硬化病变随时间的影像学、组织学、免疫组化及形态学反应。
94只兔接受动脉解剖，给予高胆固醇饮食3周，然后行PTA。在PTA前及PTA后1、3、5、7、14和28天获取动脉。PTA导致动脉径向伸展、中膜受压、壁内出血、正常动脉节段损伤以及内膜和中膜内的夹层分离。血栓填充和细胞积聚修复了夹层分离。血管成形术后3至5天观察到平滑肌细胞和巨噬细胞DNA合成达到峰值，通常发生在夹层分离处，但也见于动脉的正常节段。观察到外膜损伤以及随后的外膜细胞增殖和胶原生成。血管造影显示，术后3天最小管腔直径迅速减小，这是由于血管回缩或血栓填充夹层分离所致。在7至14天，管腔丢失仅有24%至33%是由内膜面积增加引起的，内膜中有22%至28%为新生内膜。
动脉粥样硬化性动脉再狭窄是由内膜增殖、血管重塑/伤口收缩以及动脉正常节段回缩等多种因素共同作用所致。动脉粥样硬化血管对PTA损伤的变异性源于夹层分离、血栓形成、细胞对损伤的反应以及瘢痕收缩和弹性回缩的变异性。
