激光血管成形术后血管的形态学变化

用腹主动脉内膜球囊损伤造成狭窄≥50％的日本大耳白兔50只进行激光血管成形术(LA),术后3、7、14、21、28、35、42、49、56和63天血管取材切片作病理变化分析。结果:LA后14天,血管平滑肌细胞(SMC)出现增殖,动脉中层SMC向内层迁移;LA后28天,内膜层SMC增殖最为明显,并导致血管再狭窄;内膜层SMC表型与合成型SMC相似;LA后35天,内膜层增厚速度降低。结论:实验性LA后SMC增殖反应呈一动态过程,与球囊血管成形术后再狭窄的病理变化大致相同,故本实验模型适于LA后血管再狭窄机制的研究。     

兔腹主动脉球囊成形术后狭窄过程中内皮素的动态变化

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、22d)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15～22d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。     

32P液体球囊血管内照射预防血管成形术后再狭窄

目的 探讨^32P液体球囊血管内近距离照射治疗对防止血管成形术后再狭窄的量效关系及其抑制再狭窄发生的可能机制。方法 27只雌性大白兔据动脉球囊扩张损伤后，实验组(18只)分别给予3、9、18和36Gy^32P液体球囊行内照射治疗，对照组(9只)灌注生理盐水。术后于不同时间点取材，行HE染色、增殖细胞核抗原(PCNA)免疫组织化学染色以及电镜观察血管组织形态学的改变，用计算机图像分析法测量管腔面积和内膜面积。结果 对照组血管内膜明显增生，管腔变狭窄。18Gy组血管壁平滑肌细胞增殖明显受抑，细胞凋亡增加，管腔面积无明显丢失；36GY组血栓形成明显；3和9Gy组均未观察到明显的生物效应。结论 ^32P液体球囊血管内照射可防止血管成形术后再狭窄发生，其机制可能为抑制血管壁平滑肌细胞增殖，促进其凋亡及改善血管重塑形。     

光学相干层析成像技术判断大鼠动脉球囊损伤后再狭窄程度

目的探讨光学相干层析成像技术(optical coherence tomography,OCT)判断大鼠动脉球囊损伤后再狭窄程度的可行性。方法将60只雄性SD大鼠随机分成对照组(假手术组30只)和实验组(球囊损伤30只),每个时间点(造模前、造模后2、7、14和28 d)取6只,制备大鼠颈总动脉球囊导管扩张损伤模型,在各个时间点将动脉组织行OCT检测并和血清学指标(LDL、HDL、ALP、CRP)、病理学指标(血管内膜与中膜厚度比值、管腔狭窄率)相比较。结果实验组血清学指标(LDL/HDL、ALP)及病理学指标都随着造模时间逐渐加重,对照组处理前后无明显变化,两组相比差别具有显著意义(P<0.05)。实验组OCT图象散射系数(μs)随造模时间逐渐增大,对照组μs处理前后无明显变化,两组相比差别具有显著意义(P<0.05);实验组μs与病理学指标(血管内膜与中膜厚度比值、管腔狭窄率)均存在高度相关性(P<0.01)。结论 OCT是评估动脉球囊损伤后再狭窄程度的可行方法。     

血管成形术后外膜细胞表型转化和迁移的实验研究

目的观察和分析血管成形术后血管外膜成纤维细胞表型转化和外膜细胞向血管内膜的迁移。方法改良导丝法损伤24只大鼠颈总动脉(CCA),制作血管再狭窄模型;采用5-溴,2尿苷嘧啶(BrDU)标记增殖和迁移的成纤维细胞,以免疫组化,BrDU单染结合α-肌动蛋白(α-actin)复染,光镜、扫描电镜和图像分析仪观察和分析损伤后3、7、14和28d,血管外、中和内膜上与BrDU结合的成纤维细胞的动态分布。结果1.免疫组化染色:BrDU结合的外膜成纤维细胞在术后第3天外膜上分布较多,至第7天达到峰值并表达α-actin,成纤维细胞发生表型转化成为成肌纤维细胞,细胞外基质(ECM)沉积;第14天,外膜上阳性细胞数下降,中膜和内膜上数量显著上升,内膜增厚,管腔狭窄;第28天,外膜、中膜和内膜阳性细胞数量回归到基线,但内膜ECM沉积较多,内膜仍增厚,管腔狭窄。不同时间点,血管三层结构内阳性细胞数比较均有显著差异(P<0.05)。2.电镜观察:血管成形术后,成纤维细胞胞质饱满,粗面内质网发达,表面分泌颗粒丰富,合成大量微丝束,转化为成肌纤维细胞;第7和14天,成肌纤维细胞形成宽大的伪足,分别伸向血管外弹力板窗孔和内弹力板窗孔,细胞呈腔内方向迁移趋势。结论血管成形术后血管外膜成纤维细胞发生表型转化,合成分泌α-actin;外膜成纤维细胞转化为成肌纤维细胞,向血管内膜迁移、增殖,成为新生内膜的细胞成分;外膜细胞和血管再狭窄有关。     

高胆脂血症兔血管再狭窄模型动脉β内照射诱导平滑肌细胞凋亡及减少中膜细胞构成

目的 :几种经皮冠状动脉血管成形术后再狭窄动物模型均表明 ,电离辐射对动脉损伤后新内膜的增生有较强的抑制作用 ,这一观点最早被认为和平滑肌细胞有丝分裂活性降低有关。本研究用于评价血管 β内照射对动脉壁平滑肌细胞密度及凋亡的影响。方法 :利用 Baum gartner技术获得高胆脂血症新西兰大白兔的损伤性颈动脉 2 5根和 7根髂动脉 ,在球囊损伤后给予 18Gy的 90 Yβ内照射 ,其结果与单纯损伤未经照射的对照组进行比较。损伤后第 8天、第 2 1天和 6周时 ,利用计算机自动处理软件分析中膜平滑肌细胞密度和凋亡细胞比例 ,凋亡细胞通过原位末…     

^192Ir高线量率血管腔内照射对抑制兔血管平滑肌细胞增殖及新生内膜过度增生的研究

目的 研究^192I搞线量率血管腔内照射对用切割球囊导管行经皮血管腔内成形术（PTA）后的日本白兔髂动脉平滑肌细胞增殖抑制的经时反应和效果。方法 20只日本白兔经左侧颈总动脉放置切割球囊导管行髂动脉PTA术，随机于一侧髂动脉施行12Gy剂量的血管腔内照射，非照射侧作为对照侧。实验动物于术后1、2、3、4、8及12周处死。根据新生内膜的形成情况，血管成形术后接受血管腔内照射的血管段按时间分为3组：即1周组5只、2－4周组9只、8－12周组6只。随后对标本进行了组织病理、形态学测量和免疫组织化学分析。结果 1周时，与照射侧比较，对照侧血管段创口修复处可明显的新生内膜增生，新生内膜中抗增殖细胞核抗原（PCNA）阳性细胞率呈一峰值；2－4周期间，与对照侧比较，照射侧血管段新生内膜增生明显减弱（P＜0．01），新生内膜中PCNA阳性细胞率较对照侧低，差异有显著性意义（P＜0．01）；8－12周，照射侧血管段增生的新生内膜较对照侧仍处较低水平，新生内膜中PCNA阳性细胞率约低于1％。经抗平滑肌细胞α胶原免疫组织化学染色，证实新生内膜中主要为平滑肌细胞。结论 由照射所致的新生内膜增生过程的抑制作用从开始时即已启动。12Gy的^192Ir高线量率照射能有效地抑制用切割球囊导管损伤引起的日本白兔髂动脉新生内膜的过渡增生。     

糖尿病足介入治疗17例回顾性分析

目的：评价糖尿病下肢动脉的血管改变及血管内介入治疗的临床价值。方法：对36例糖尿病足行下肢动脉DSA检查，并同时与血管超声进行对照。其中17例节段性狭窄行介入治疗(12例经皮血管球囊成形术，5例血管腔内支架植入)。术后常规抗凝治疗，并于6个月后血管造影复查。结果：糖尿病足下肢动脉有不同程度的狭窄与阻塞同时存在，细小动脉多有闭塞；17例行介入治疗者均有胭动脉以上动脉的慢性损伤。介入治疗可以改善糖尿病足下肢动脉的血液灌注，通过控制血糖和改善血液循环，其治疗的近期疗效令人满意。结论：DSA检查可以准确了解阻塞部位及程度，对糖尿病足的下肢动脉介入治疗疗效满意，可以大大降低患者的病残率。     

血管内支架成形术治疗椎基底动脉狭窄

目的 初步总结应用血管内支架成形术治疗椎基底动脉狭窄的经验，探讨其适应证，技术要点和围手术期处理。方法 20例表现为反复的短暂性脑缺血发作或既往有后循环梗塞病史，13例为反复头晕发作或血管性头痛。椎动脉起始段13例：椎动脉颅外段3例，颅内段5例；基底动脉12例。病变狭窄程度均在70％以上，狭窄长度2－12mm。所有患者接受血管内支架成形术治疗，将球囊膨胀型支架（BX，AVES670，EXPRESS，BIODIVESO）在微导丝导引下通过狭窄部位，缓慢充盈球囊，造影观察支架释放情况后缓慢回撤球囊。结果 29例恢复正常管径，4例狭窄程度减小80％以上，无内膜撕裂和血栓形成。临床随访3－10个月，所有患者均恢复满意，无短暂性缺血再发生或卒中；影像学随访10例患者，均无血管再狭窄。结论 椎基底动脉狭窄的血管内支架成形术治疗椎基底动脉狭窄是一种有效，安全的方法，但远期疗效仍需要进一步随访。     

PCI后新生血管内膜的形成和增生及其机制——血管紧张素Ⅱ及其受体作用的实验研究

目的　本项目通过建立球囊损伤大鼠髂动脉制作内膜增生模型 ,对体外培养的VSMC生物学特性进行检测 ,采用ATR基因转染VSMC等技术 ,在器官、细胞、亚细胞、分子水平探讨RAS主要成分AngⅡ及其受体亚型在PCI后新生血管内膜形成和增生中的作用 ,重点研究AngⅡ及其受体亚型在VSMC迁移、增生和凋亡中的作用及其机制 ,为临床应用抑制RAS的方法防治RS提供确切的理论依据。方法　①在体动物实验 :用球囊损伤方法制作大鼠髂动脉损伤后内膜增生的动物模型 ,利用受体放射性配基结合分析方法、电镜、原位杂交及流式细胞术等技术 ,并以此实验平台研究比较增生内膜中RAS有关成份活性变化、AngⅡ受体表达变化、VSMC增殖和凋亡特性变化 ,以了解这些变化与内膜增生的关系。②细胞学实验 :通过体外培养VSMC研究不同AngⅡ浓度以及干预剂作用等条件下AngⅡ受体表达变化 ,了解其变化对VSMC增殖、迁移和凋亡等生物学行为的影响 ,特别是对近年来受到重视的VSMC迁移的影响作用。③基因转染研究 :通过构建AT2 R基因的腺病毒载体转染体外培养的大鼠主动脉VSMC ,建立表达AT2 R的细胞模型 ,研究VSMC表达AT2 R后其生...     

大鼠颈动脉球囊损伤后血管平滑肌细胞过度增殖与基质交感分子1的关系研究

目的研究大鼠颈动脉球囊损伤后血管平滑肌细胞中基质交感分子1(STIM1)的表达变化情况,揭示平滑肌细胞增殖的内在机制。方法采用大鼠颈动脉球囊损伤后血管再狭窄的动物模型,18只SD大鼠随机均分为3组:对照组、损伤7d组和损伤14d组。免疫组织化学染色和反转录-聚合酶链反应(RT-PCR)检测增生的血管平滑肌细胞中STIM1的表达变化,HE染色评价血管增生情况。结果正常大鼠颈动脉内膜与中膜面积比值(IA/MA)很小,损伤7d组IA/MA值显著高于对照组(P<0.05);损伤14d组IA/MA值显著高于7d组(P<0.05)。损伤后7d血管壁STIM1 mRNA水平显著高于对照组(P<0.05);损伤后14d血管壁STIM1 mRNA显著高于7d组(P<0.05)。免疫组化显示STIM1在血管壁的表达主要位于增殖的平滑肌细胞中,随损伤时间延长其表达量逐渐升高。结论颈动脉球囊损伤后血管平滑肌细胞增殖伴有STIM1表达的上调,STIM1可能参与对血管平滑肌细胞增殖的调控。     

颈动脉粥样硬化斑块动物模型的MRI评价

目的:利用新西兰兔建立颈动脉粥样硬化模型,探索颈动脉粥样硬化斑块模型建立的可行性,并通过MR特殊线圈检测斑块,与病理对照观察斑块的MRI表现,为进一步研究颈动脉粥样硬化斑块与脑缺血的关系奠定基础。材料和方法:利用高脂饮食饲养成年兔20只,饲养前均行颈动脉检查,作为正常对照。8周后,在DSA辅助下经球囊损伤一侧颈动脉内膜,造影观察到内壁毛糙后停止操作。7d后行MR扫描观察颈动脉管壁信号变化。继续高脂饲养2个月后,多次行颈动脉MR检查,最后取病理对照。结果:20只兔饲养至3周时由于各种原因死亡4只,行球囊拉损术时死亡4只,其余12只均造模成功,成功率为75%(12/16)。第一次MRI显示管壁T_1WI、PDWI及T_2WI均为高信号,第2-6次MRI检查显示管壁内膜明显增厚,病理显示管壁内膜下局部泡沫细胞明显增多,同时平滑肌细胞积聚,形成类似于人类病变的粥样斑块。结论:高脂饮食饲养后行颈动脉球囊拉损制作兔颈动脉粥样硬化斑块是切实可行的办法,MRI是良好的检测颈动脉损伤和显示颈动脉斑块的方法。     

Evaluation of Arterial Impairment after Experimental Gelatin Sponge Embolization in a Rabbit Renal Model

ObjectiveArterial stenosis is a major obstacle for subsequent interventional procedures. We hypothesized that the stenosis is caused by gelatin sponge embolization and performed an experimental study in a rabbit renal model.ResultsGelatin sponge particles were mainly observed in the segmental and interlobar arteries. Transmural inflammation of the embolized arterial wall and mild thickening of the media were observed 1 week after embolization. Resorption of the gelatin sponge and organization of thrombus accompanied by foreign body reactions, were observed from 2 to 4 weeks after embolization. Microscopic images of the 3 weeks group showed vessel lumens filled mostly with organized thrombi, resulting in severe stenosis. Additionally, vessels showed a thickened intima that contained migrating smooth muscle cells and accompanying interruption of the internal elastic lamina. The migrating smooth muscle cells were distributed around the recanalized arterial lumen.ConclusionGelatin sponge embolization may induce arterial stenosis by causing organized thrombus and intimal hyperplasia, which consists of migrating smooth muscle cells and intimal collagen deposits.     

激光热消蚀兔颈动脉增生修复的形态学观察

本实验用Ｎｄ：ＹＡＧ激光经金属帽光纤传输，在１８只健康兔颈总动脉造成急性热损伤，于消蚀后即刻至８周动态观察血管壁组织增生修复变化，结果表明，激光消蚀后出现炎症反应和血小板粘附聚集，２周时内皮层恢复正常，但中膜平滑肌细胞呈过度增殖，管腔狭窄和闭塞。此可能是激光血管成形术后再狭窄的机制之一。     

A rabbit model of atherosclerosis at carotid artery: MRI visualization and histopathological characterization

To induce a rabbit model of atherosclerosis at carotid artery, to visualize the lesion evolution with magnetic resonance imaging (MRI), and to characterize the lesion types by histopathology. Atherosclerosis at the right common carotid artery (RCCA) was induced in 23 rabbits by high-lipid diet following balloon catheter injury to the endothelium. The rabbits were examined in vivo with a 1.5-T MRI and randomly divided into three groups of 6 weeks (n=6), 12 weeks (n=8) and 15 weeks (n=9) for postmortem histopathology. The lesions on both MRI and histology were categorized according to the American Heart Association (AHA) classifications of atherosclerosis. Type I and type II of atherosclerotic changes were detected at week 6, i.e., nearly normal signal intensity (SI) of the injured RCCA wall without stenosis on MRI, but with subendothelial inflammatory infiltration and proliferation of smooth muscle cells on histopathology. At week 12, 75.0% and 62.5% of type III changes were encountered on MRI and histopathology respectively with thicker injured RCCA wall of increased SI on T(1)-weighted and proton density (PD)-weighted MRI and microscopically a higher degree of plaque formation. At week 15, carotid atherosclerosis became more advanced, i.e., type IV and type V in 55.6% and 22.2% of the lesions with MRI and 55.6% and 33.3% of the lesions with histopathology, respectively. Statistical analysis revealed a significant agreement (p<0.05) between the MRI and histological findings for lesion classification (r=0.96). A rabbit model of carotid artery atherosclerosis has been successfully induced and noninvasively visualized. The atherosclerotic plaque formation evolved from type I to type V with time, which could be monitored with 1.5-T MRI and confirmed with histomorphology. This experimental setting can be applied in preclinical research on atherosclerosis.     

异物创伤性动脉瘤犬模型构建的初步探讨

目的：建立异物创伤性动脉瘤的犬模型,为伴血管损伤软组织异物一站式介入治疗研究提供动物模型。 方法：随机选取2年龄的健康雄性比格犬7只,分为颈动脉瘤造模5只和未造模2只,造模于右侧颈动脉共5支血管为研究组,其左侧颈动脉及未造模2只犬两侧颈动脉共9支血管为对照组。研究组将长约15~20 mm的离断颈静脉剪开、缝合于同侧颈总动脉前璧上,以弯型断针穿破静脉片及动脉前壁,静脉片-动脉壁间腔搏动性充盈且无缝缘渗漏后,断针部分留存于该间腔甚或动脉腔内,逐层缝合手术区域组织。然后,经皮经股动脉插管选择性颈总动脉进行数字减影血管造影（DSA）。对照组颈动脉仅于其旁以缝针经皮扎伤软组织且无明显出血及血肿。术前、术后行颈部CT血管成像（CTA）和数字放射摄影（DR）检查与评估。 结果：研究组5支右侧颈动脉断针创伤性动脉瘤均成功造模,技术成功率100%;DSA清晰显示动脉破口、动脉瘤状动脉突起及断针异物,载瘤动脉局部轻度痉挛及狭窄,创伤性动脉瘤模型的瘤颈宽度为（2.1±1.3）mm,瘤体宽（9.7±1.1）mm,瘤体高（4.2±1.7）mm;CTA不如DSA显示效果佳。对照组9支颈动脉均正常。 结论：采用颈静脉片侧-侧吻合于同侧颈动脉前壁上并以断针穿破静、动脉壁且断针部分留置于其间的技术与方法,成功构建了异物创伤性动脉瘤犬模型。     

Electron-microscopic study on the effect of an expandable metallic stent placement in the aortic wall]

As part of a series of basic experiments on using metallic stents for treatment of vascular stenosis, a chronological examination of changes in dog aorta following implantation of a self-expandable metallic stent was conducting using transmission and scanning electron microscopy. The Giantruco stent was placed in the abdominal aorta via the right carotid artery. One week after insertion, the aortic intima was depressed and degenerative changes observed in both endothelial and medial smooth muscle cells. After 2 weeks, except for the bend portion, the stent was covered with neointima. The neointimal surface was covered by premature endothelial cells with abundant microvilli and prominent nuclear protrusions. Under the endothelial cells, immature mesenchymal cells, such as fibroblast, were scattered throughout the edematous intercellular space. At 4 weeks, the stent was completely covered by neointima and the endothelial cells had flattened and few microvilli were in evidence. In this thickened intima, premature smooth muscle cells with myofilaments and basement membranes were observed but, around them, few collagen fibers and only occasional elastic fibers were found. At 6 weeks, the intimal surfaces were flat and smooth with a slight intimal elevation over the stent. No thrombus was observed throughout the period of the experiment. The above results indicate that dilation using metallic stents may be a useful method for treatment of vascular stenosis.     

Increased expression of nuclear NF-kappaB after coronary artery balloon injury can be inhibited by intracoronary beta-irradiation

PURPOSE: Molecular mechanisms by which balloon angioplasty injury-induced neointimal hyperplasia can be reduced by intravascular brachytherapy are unclear. We investigated the role of nuclear factor-kappaB (NF-kappaB) in neointimal hyperplasia following intracoronary irradiation. MATERIALS AND METHODS: Fifty-four coronary arteries from 30 pigs were divided into 6 groups: sham control, balloon angioplasty injury alone, beta-irradiation at doses of 14 or 20 Gy, and 14 or 20 Gy beta-irradiation immediately followed by balloon injury. Coronary arteries were injured by overstretch balloon angioplasty and then the arteries were irradiated using a Rhenium-188 ((188)Re) beta-emitting solution-filled balloon. Pigs were scarified one day or one week after coronary interventions for molecular detection and six weeks after the procedures for histological examination. RESULTS: Six weeks after coronary interventions, the histological results show that balloon angioplasty injury had induced intimal hyperplasia in coronary artery but the response was significantly reduced by 28% and 60% when the injury was immediately treated by 14 and 20 Gy (188)Re beta-irradiation, respectively. The expression of arterial NF-kappaB p65, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) were detected at one day and one week after the procedures. The treatment of balloon injury could significantly induce the NF-kappaB p65 expression in both gene and protein levels, and such induction could be significantly reduced by (188)Re beta-irradiation at dose of 20 Gy. However, the similar result on the regulation of gene expression affected by the beta-irradiation could not be observed in ICAM-1 and VCAM-1. CONCLUSION: The inhibitory effect of intracoronary brachytherapy on neointimal formation following overstretch balloon angioplasty could involve inhibition of NF-kappaB p65.     

Increased expression of nuclear NF-kappaB after coronary artery balloon injury can be inhibited by intracoronary beta-irradiation

Purpose: Molecular mechanisms by which balloon angioplasty injury-induced neointimal hyperplasia can be reduced by intravascular brachytherapy are unclear. We investigated the role of nuclear factor-kappaB (NF-κB) in neointimal hyperplasia following intracoronary irradiation.

Materials and methods: Fifty-four coronary arteries from 30 pigs were divided into 6 groups: sham control, balloon angioplasty injury alone, β-irradiation at doses of 14 or 20 Gy, and 14 or 20 Gy beta-irradiation immediately followed by balloon injury. Coronary arteries were injured by overstretch balloon angioplasty and then the arteries were irradiated using a Rhenium-188 (¹⁸⁸Re) β-emitting solution-filled balloon. Pigs were scarified one day or one week after coronary interventions for molecular detection and six weeks after the procedures for histological examination.

Results: Six weeks after coronary interventions, the histological results show that balloon angioplasty injury had induced intimal hyperplasia in coronary artery but the response was significantly reduced by 28% and 60% when the injury was immediately treated by 14 and 20 Gy ¹⁸⁸Re β-irradiation, respectively. The expression of arterial NF-κB p65, intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) were detected at one day and one week after the procedures. The treatment of balloon injury could significantly induce the NF-κB p65 expression in both gene and protein levels, and such induction could be significantly reduced by ¹⁸⁸Re β-irradiation at dose of 20 Gy. However, the similar result on the regulation of gene expression affected by the β-irradiation could not be observed in ICAM-1 and VCAM-1.

Conclusion: The inhibitory effect of intracoronary brachytherapy on neointimal formation following overstretch balloon angioplasty could involve inhibition of NF-κB p65.