关节镜下同种异体组织重建膝关节前后交叉韧带的临床研究

目的　评价关节镜下同种异体组织重建膝关节前后交叉韧带 (ACL ,PCL)的疗效。方法　回顾调查了 36例孤立性交叉韧带损伤病人 ,将其分为 2组 ,A组 :ACL损伤 2 8例 ;B组 :PCL损伤 8例。分别应用同种异体B -PT -B、半腱与股薄肌腱、胫后肌腱、跟腱 -骨和四头肌腱 -骨重建 ,平均随访 2 1 5个月。结果　Lysholm评分 :A组术前平均 6 3± 5 6 ;术后 90±5 5 ;B组术前平均 6 1± 7 6 ,术后 88± 6 0 ;两组手术前后差异显著 (P <0 0 1) ;IKDC评分 :A组A级 2例 (7% ) ,B级 16例 (5 7% ) ,C级 8例 (2 9% ) ,D级 2例 (7% ) ;B组A级 1例 (12 5 % ) ,B级 3例 (37 5 % ) ,C级 3例 (37 5 % ) ,D级 1例 (12 5 % )。KT2 0 0 0测定 :A组由术前胫骨前移平均 11 90± 0 2 7mm减少至术后 4 30± 1 4 2mm ;B组胫骨后移由术前平均 10 5± 2 5mm减少至术后 5 9± 1 5mm ,两组手术前后有显著差异 (P <0 0 1)。术后健患侧比较 :A组平均 2 3± 0 9mm ;B组 2 7± 1 3mm ;健患差异 :A组 <3mm2 3/ 2 8例 (82 % ) ,>5mm 3例 (11% ) ;B组 <3mm 5 / 8例 (6 2 5 % ) ,>5mm 2例 (2 5 % )。前后抽屉试验大部分平均恢复 1°以上 ,并呈现明显的硬终点。术后ROM ,A组 :正常 2 6 / 2 8例 (93% ) ,接近正常 2 / 2 8例 (7% ) ;B组 :     

血管外膜应用西罗莫司对静脉移植物再狭窄的作用

目的探讨血管外膜应用西罗莫司对静脉移植物再狭窄的作用。方法 12条犬建立双侧股动脉自体颈外静脉旁路移植模型,随机喷涂西罗莫司的纤维蛋白胶(200 μg／2 ml)于一侧移植静脉外表面为实验组,对侧喷涂相同剂量蛋白胶为对照组。在术后2周和4周各取6条犬双侧静脉移植物制片,计算机图像分析系统测量和计算内膜厚度和截面积;检测管壁增殖细胞核抗原阳性细胞指数(PCNAI);扫描电镜观察内膜超微结构。结果术后2周和4周实验组的内膜厚度和截面积[(168．93±50．18)μm和(175．93±54．17)μm],[(1．08±0．20)mm2和(1．23±0．34) mm2]均较对照组[(201．83±43．57)μm和(224．83±45．92)μm)]和[(1．48±0．11)mm2和 (1．71±0．15)mm2]降低,P<0．05。术后2周后实验组血管壁PCNAI较对照组降低(14．78±1．89 和23．56±1．87,P<0．05),术后4周两组差异无统计学意义。扫描电镜下见术后2周实验组内皮覆盖较对照组良好,术后4周两组内膜已经完全内皮化。结论血管外膜局部应用西罗莫司对预防静脉移植物术后早期狭窄有良好的作用。     

腹腔镜下改良子宫肌瘤切除术91例临床分析

目的　探讨腹腔镜下改良子宫肌瘤切除术的手术技巧和疗效。　方法　通过对子宫切口设计、组织分离 剥离器使用、肌瘤营养血管处理等手术技巧和手术器械的改进 ,行腹腔镜下子宫肌瘤切除术 91例。根据术前B超检测 ,分成肌瘤径线≥ 70mm组和 <70mm组。　结果　术中共发现肌瘤 10 2个 ,其中肌壁间肌瘤 73个 (71 6 % )。手术时间为 (116 1± 4 5 7)min ,出血量 (81 7± 4 1 7)ml,术后住院时间 (8 0± 2 8)天 ,术后最高体温 (37 9± 0 5 )℃。肌瘤径线≥ 70mm组术中出血量 (95 2± 4 2 0 )ml ,<70mm组 (6 5 6± 31 7)ml(t=2 35 ,P <0 0 5 ) ;两组手术时间分别为 (119 1± 4 4 2 )min和 (112 9± 33 4 )min ,(t=0 6 9,P >0 0 5 )。　结论　腹腔镜改良子宫肌瘤切除术可缩短手术时间、减少术中出血 ,即使较大径线的子宫肌瘤也能达到较好的疗效。     

缺血预处理对大鼠移植肝脏保存再灌注损伤的保护及机制探讨

目的探讨缺血预处理 (ischemicpreconditioning ,IP)对大鼠移植肝脏保存再灌注损伤的保护作用及机理。方法采用SD大鼠原位肝移植动物模型 ,12 8只大鼠随机分成A(对照组 )、B(IP组 )、C(腺苷 ,Ado组 )、D(NO合成抑制剂 ,NAME组 )组 ,每组 32只。其中各组的半数用于观察存活率 ,另一半用于移植肝脏再灌注 2h后取血及肝脏检测。结果IP组和Ado组的 1周存活率、血清NO水平及肝组织腺苷含量分别为 88% (7/ 8)和 88% (7/ 8) ,(33 0± 6 1) μmol/l和 (2 9 1± 6 5 ) μmol/l,(7 2± 1 8) μmol/g和 (5 7± 1 3) μmol/g ,均高于对照组的 38% (3/ 8) ,(15 4± 3 0 )mol/L和 (3 6 9±0 5 4 ) μmol/g (P <0 0 5 ) ,血清ALT及TNF含量分别为 (2 87± 82 )IU/L和 (35 7± 93)IU/L ,(1 15± 0 2 3)ng/ml和 (1 14± 0 2 7)ng/ml,均低于对照组的 (5 88± 5 8)IU/L及 (1 5 9± 0 35 )ng/ml(P <0 0 5 ) ,组织的病理学改变也轻于对照组 ;NAME组的 1周存活率、血清NO及ALT含量等分别为 2 5 % (2 / 8)、(13 74± 3 11) μmol/l及 (6 34± 6 5 )IU/L ,与对照组相近 (P >0 0 5 ) ,而肝组织腺苷含量为 (5 5 6± 1 19)μmol/g ,与对照组差异有显著意义 (P <0 0 5 )。 结论IP对大鼠移植肝脏的保存再灌注损伤具有保护     

扩张压力对兔颈外静脉移植物再狭窄的影响

目的　研究不同扩张压力对兔颈外静脉内皮完整性及颈外静脉桥再狭窄的影响。方法　 1 8只NZW兔 ,随机分为A、B、C组。每组兔颈外静脉分别以 50、1 0 0和 2 0 0mmHg(1mmHg=0 .1 33kPa)扩张 ,静脉内银染铺片法和扫描电镜进行内皮完整性评分。扩张后行颈外静脉颈总动脉移植 ,2 8d后测定静脉桥管腔面积和内膜厚度。结果　A组内皮完整性评分 (1 .42 )显著低于B组 (2 .67,P <0 .0 1 )和C组 (3 .83 ,P <0 .0 1 )。A组的静脉桥的管腔面积 (1 1 .3± 2 .0 )mm2 显著大于B组 [(6 .0± 1 .7)mm2 ,P =0 .0 0 1 ]和C组 [(4.5± 1 .2 )mm2 ,P <0 .0 0 1 ] ;A组的静脉桥的内膜厚度 (36 .2± 3 .4) μm显著小于B组 [(52 .3± 7.7) μm ,P =0 .0 0 1 ]和C组 [(53 .1± 5 .8) μm ,P <0 .0 0 1 ]。结论　 50mmHg的扩张压力引起的兔颈外静脉桥再狭窄的程度明显轻于 1 0 0mmHg和2 0 0mmHg,其原因在于能较好地保存静脉内皮完整性     

肿瘤坏死因子α介导骨骼肌缺血-再灌注损伤的实验研究

目的研究肿瘤坏死因子α(TNF α)介导骨骼肌缺血 再灌注损伤的作用机制。方法2 4只健康雄性SD大鼠 (2 5 0～ 30 0g)随机分成 3组。对照组 :仅行麻醉及颈外静脉插管术 ;损伤组 :左后肢缺血 4h ,再灌注 4h ;治疗组 :缺血 4h ,再灌注 4h ,再灌注即刻经静脉导管给与抗TNF α单克隆抗体。结果损伤组较对照组单核细胞TNF αmRNA转录增加 ,血浆丙二醛 (MDA) (9 9± 1 8)比(5 5± 0 4 )、肌酸激酶 (CK) (12 2± 2 4 )比 (49± 11)、一氧化氮 (NO) (2 70± 98)比 (12 8± 4 6 )、组织过氧化物酶 (MPO) (骨骼肌 4 2 7± 0 5 3)比 (1 2 8± 0 19,肺 2 6 1± 0 12 )比 (0 5 7± 0 0 2 )显著升高 (P <0 0 1) ,骨骼肌和肺组织超微结构发生病理改变。治疗组较损伤组MDA(6 2± 1 2 )比 (9 9± 1 8)、CK(5 8±12 )比 (12 2± 2 4 )、NO(15 4± 5 5 )比 (2 70± 98)、MPO(骨骼肌 2 13± 0 2 1)比 (4 2 7± 0 5 3肺 0 95± 0 0 1)比(2 6 1± 0 12 )水平明显降低 (P <0 0 5 ) ,骨骼肌和肺组织病理损伤减轻。结论骨骼肌缺血 再灌注激发TNF α的生成 ,在介导骨骼肌和肺的损伤中起重要作用     

远端脾肾静脉分流术后肝外门静脉血流动力学变化的实验研究

目的　探求健康犬远端脾肾静脉分流术后肝外门静脉血流动力学变化。方法　插管连续测量犬的远端脾肾静脉吻合术前后自由门静脉压力、脏侧闭塞门静脉压力、平均动脉压 ,并应用公式通过上述三个压力参数计算出肝外门体分流率。结果　自由门静脉压术前为 10 .15± 1.6 5 mm Hg,术后为 10 .0 0± 2 .4 1m m Hg,仅下降 0 .0 7± 2 .4 1mm Hg,(t=0 .10、0 .4>P>0 .2 )无显著差异 ,脏侧闭塞压术前 6 5 .71± 5 .11m m Hg,术后为 4 6 .6 2± 8.35 mm Hg,下降 19.10± 10 .4 5 mm Hg(t=6 .35 ,p <0 .0 0 1) ;平均动脉压术前为 133.76± 17.0 7m m Hg,术后为 10 2 .4 1± 2 0 .0 0 mm Hg,下降 31.35± 2 2 .18m m Hg(t=4 .89,P<0 .0 0 1) ;门体分流率术前为 8.5 0 %± 2 .13% ,术后为 13.16 %± 4 .18% ,增加了 4 .5 3%± 4 .0 9% (t=3.83,P<0 .0 0 5 ) ;脏侧闭塞压与门静脉自由压之差术前为 5 5 .6 4± 6 .2 4 m m Hg,术后为 36 .6 2± 8.35 mm Hg,下降 19.0 2± 10 .38mm Hg(t=6 .37,P<0 .0 0 1)。结论　门静脉系统中存在功能分区 ,即门脉肠系膜区和胃脾区 ,且二者之间存在功能屏障力 ;Warren's手术具有理论基础     

扩张皮肤血液动力学及皮瓣移植实验研究

目的　研究扩张皮肤血液动力学变化规律 ,探索将扩张皮肤设计成任意皮瓣进行皮肤移植的最佳时机。方法　以 72只兔耳为活体实验标本 ,应用微循环显微图像计算机分析系统、酶组织化学染色和多功能真彩色病理图像分析技术 ,观测不扩张对照耳 (n =8)皮肤与处于不同扩张时间的扩张组 (n =8× 8)皮肤内微血管直径、密度、血流速度、血流量等指标值 ,并将扩张皮肤设计成任意皮瓣移植 ,测量皮瓣成活部分的长宽比例和面积。结果　 ( 1)扩张皮肤微血管直径 ( 13 4 3± 0 98)μm、密度 ( 0 0 4 72± 0 0 0 2 2 )、血流速度 ( 10 12 70± 65 5 1) μm/s、血流量 ( 14 71± 0 74 ) μm3/s ,较对照皮肤 [(分别是 ( 7 2 2± 0 71) μm、( 0 0 10 8± 0 0 0 0 2 )、( 3 2 7 0 1± 65 5 1) μm/s、( 1 4 6± 0 4 1) μm3/s]明显增大变快 ,差异有显著意义 (t=6 4 9～ 4 9 4 9,P均 <0 0 1)。 ( 2 )扩张过程中 ,血流速度加快并一直维持在较高水平 ;血管直径和血流量每 4周有 1次周期性变化 ,每 1周期的第 3周末均出现一增量峰值 ,后一周期的变化是在前一周期增量基础上的进一步增大 ;血管密度也呈周期性变化 ,但各周期间密度变化范围相同。 ( 3 )每一变化周期第 3周末的扩张皮肤设计成任意皮瓣移植 ,与同一周     

缺血预处理和阿霉素预处理对大鼠肝脏低温保存损伤的保护作用

目的研究预处理对大鼠肝脏低温保存损伤的保护作用。方法应用大鼠肝脏离体非循环灌注模型 (IPRL) ,对供肝分别作缺血预处理 (IPC)和阿霉素预处理 (DPC) ,比较各组供肝低温保存损伤的程度。结果流出液中AST和ALT的酶学水平 ,IPC组 (40 1± 6 3、17 1± 0 5 )U L和DPC组 (43 6± 3 7、19 4± 0 8)U L显著低于未预处理 (NPC)组 (6 4 5± 8 2、2 3 8± 3 9)U L(P <0 0 5 ) ;胆汁分泌量及肝组织ATP含量 ,IPC组 (5 3 5± 10 2 ) μl、(6 2± 0 6 ) μmol g和DPC组 (5 0 5± 8 1) μl、(6 0±0 6 ) μmol g显著高于NPC组 (2 2 8± 9 7) μl、(2 6± 0 3) μmol g(P <0 0 5 ) ;肝组织丙二醛 (MDA)的含量 ,IPC组 (4 36± 0 2 6 )nmol g和DPC组 (4 5 1± 0 13)nmol g显著低于NPC组 (6 75± 0 17)nmol g(P<0 0 5 ) ;光镜及电镜结果显示 ,IPC组和DPC组肝细胞损伤的程度显著轻于NPC组 ;而IPC组与DPC组相比较 ,上述指标均无显著性差异 (P >0 0 5 )。结论预处理对供肝低温保存损伤具有明显的保护作用 ,药物预处理可以模拟IPC的效果。药物预处理为临床提供一种安全有效的预处理方法。     

内皮抑素对胃癌抑制作用的实验研究

目的　研究内皮抑素对胃癌生长和转移的抑制作用 ,并探讨其对胃癌细胞凋亡的影响。方法　建立人胃腺癌裸鼠原位种植转移模型。将 72只荷瘤裸鼠随机分成 4组 ,对照组 3 6只 ,治疗各组每组 12只。种植后第 1周开始皮下注射内皮抑素 ,隔天 1次 ,剂量为 0mg/kg(对照组 )、2 5mg/kg、10 0mg/kg、2 0 0mg/kg(治疗组 ) ,共用 7周。种植后第 8周处死动物 ,测量原位肿瘤体积、抑瘤率、肿瘤微血管密度 (MVD)、肿瘤细胞凋亡指数 (AI) ,观察肿瘤细胞腹膜、肝、其他脏器转移及腹水情况。结果　内皮抑素剂量为 0mg/kg、2 5mg/kg、10 0mg/kg、2 0 0mg/kg时 ,原位肿瘤体积分别为 ( 15 83±5 76)mm3、( 5 91± 3 84 )mm3、( 65 7± 4 3 1)mm3、( 1 89± 1 0 2 )mm3;抑瘤率分别为 0、62 7%、95 8%、99 9% ;MVD分别为 ( 13 70± 3 90 )、( 5 73± 2 3 6)、( 2 17± 1 2 8)、( 0 66± 0 2 5 ) ;AI分别为 ( 3 91±2 5 8) %、( 6 76± 5 0 3 ) %、( 18 92± 6 75 ) %、( 2 8 5 7± 10 3 4 ) % ;腹膜转移率分别为 87 1%、5 4 5 %、16 7%、0 ;肝转移率分别为 83 9%、2 7 3 %、8 3 %、0。治疗组与对照组相比 ,组间胃癌生长和转移的抑制作用差异有显著性意义 (t=3 1 77,P <0 0 5 ) ,且抑制作用与内皮抑素     

静电纺丝血管外支架抑制静脉移植物内膜增生

目的 探讨聚-3-羟基丁酸与聚-4-羟基丁酸聚酯[P(3HB-co-4HB)]静电纺丝血管外支架预防静脉移植物内膜增生的机制.方法 静电纺丝技术制备P(3HB-co-4HB)血管外支架.SD大鼠随机分成2组,每组24只,建立颈外静脉-颈总动脉血管移植模型:无支架(Ns)组和非限制支架(PS)组.分别于术后3、7、14、28 d取静脉移植物标本,计算机图像系统分析内膜、中膜厚度和面积,免疫组织化学检测静脉移植物增殖细胞核抗原(PCNA)表达.逆转录-聚合酶链反应(RT.PCR)检测静脉移植物血小板源性生长因子.BB(PDGF-BB)和组织因子(TF)mRNA表达.结果 术后7、14、28 d支架组静脉移植物内膜与中膜的厚度和面积明显低于无支架组(P<0.05).两组PCNA表达均增加并在术后14 d最高,而支架组在术后7、14 d PCNA表达低于无支架组(P<0.05).术后3、7d支架组PDGF.BB和TFmRNA表达明显低于无支架组(P<0.01).结论 静电纺丝P(3HB-co-4HB)血管外非限制性支架能抑制静脉移植物内膜增生,并通过降低静脉移植物管壁早期组织因子表达发挥作用.     

大鼠自体静脉移植后内膜增生与细胞外基质堆积的研究

目的:研究静脉移植术后内膜增生(IH)中细胞基质(ECM)堆积的发生、发展及与平滑肌细胞(SMC)增殖的关系.方法:将大鼠一段颈外静脉桥接移植入颈总动脉,运用组织切片的特殊染色及免疫组化方法,观察术后1天至24周移植静脉的IH中,Ⅰ型胶原(ColⅠ)、Ⅱ型胶原(ColⅢ型)及SMC结蛋白(D_m)的变化.结果及结论:术后2周,IH中开始出现胶原的堆积,术后12周,IH中胶原含量达最大值并自此保持稳定不变,术后24周IH主要由细胞外基质组成;术后2周,IH中SMC的D_m开始表达,表明SMC的表型开始由收缩型向分泌型改变,术后6周,D_m达最大值,表明此时分泌型SMC最多,SMC可能是分泌细胞外基质的间质效应细胞.     

Differential, time-dependent effects of perivenous application of fibrin glue on medial thickening in porcine saphenous vein grafts.

OBJECTIVE: Neointimal and medial thickening play a critical role in late vein graft failure following CABG. Previous ex vivo experiment suggested that perivenous application of fibrin glue may reduce the damage in the circular smooth muscle cell layer of the media of the vein graft shortly after exposing to arterial pressure. However, the in vivo as well as the longer term impact of this intervention remain unknown. METHODS: Bilateral saphenous vein-carotid artery interposition grafting was performed in eight large white pigs (35-45 kg). In each pig, one of the grafts was randomly selected to receive perivenous fibrin glue support while the contralateral graft served as control. At 1 and 4 months following surgery (n=4 pigs in each group), all 16 patent vein grafts were removed and pressure-fixed. Multiple histological sections from each graft were prepared. Proliferating cell nuclear antigen (PCNA) was detected by immunocytochemistry. Vein graft morphology was assessed using computer-aided planimetry. RESULTS: Although perivenous application of fibrin glue had little effects either on medial thickness 1 month after implantation or on PCNA index, it significantly increased medial thickness (control: 0.37+/-0.02 mm; treated: 0.55+/-0.02 mm, p<0.001) and total wall thickness (control: 0.75+/-0.04 mm; treated: 0.92+/-0.04 mm, p=0.008) at 4 months (mean+/-SEM; n=4 in each group). CONCLUSIONS: Our data indicated that perivenous application of fibrin glue enhances graft thickening and as such does not constitute a strategy for preventing late vein graft failure after CABG.     

Association of smooth muscle cell phenotypic modulation with extracellular matrix alterations during neointima formation in rabbit vein grafts.

PURPOSE: To clarify the mechanisms of structural changes underlying vein graft stenosis that limits efficacy of bypass grafting operation, we examined the accumulation and distribution of various extracellular matrix (ECM) components during neointima formation in rabbit vein grafts and analyzed their correlation with proliferation and phenotypic modulation of smooth muscle cells (SMCs). METHODS AND RESULTS: An autologous external jugular vein graft was transplanted into the carotid artery in 25 rabbits. After the restoration of blood flow, the graft was markedly dilated. Medial SMCs in the graft appeared to be injured, and they began to proliferate at day 4 and subsequently migrated and formed the neointima at day 7. The neointima observed at days 7 and 14 contained ECM components, including type I collagen, heparan sulfate, and chondroitin sulfate, and the intimal SMCs were phenotypically modulated from the differentiated-type (SM2-positive and SM embryonic-negative) to the dedifferentiated-type (SM2-negative and SM embryonic-positive) as determined with immunostainings for myosin heavy chain isoforms. The intimal SMC proliferation was maximal at 2 weeks and then decreased rapidly. However, the neointima continued to thicken thereafter throughout the 6-month period of the experiment, and ECM accumulation, such as type I collagen and decorin, a small dermatan sulfate proteoglycan, was a prominent feature observed in the hypocellular region of the deep intima from 2 months after the transplantation. The phenotype of the intimal SMCs gradually returned to the differentiated-type from the deep intima after 2 months, but a small number of the intimal SMCs remained in the dedifferentiated phenotype even at 6 months after the operation. CONCLUSION: The neointima in the vein graft was formed initially by means of migration and proliferation of the phenotypically modulated, dedifferentiated-type SMCs and continued to thicken by means of sustained ECM accumulation, including type I collagen and decorin, in association with the prolonged presence of the dedifferentiated-type SMCs. These chronologic features in cell kinetics and ECM accumulation may contribute to the frequent occurrence of graft wall thickening that occurs in the vein grafts.     

三七总皂苷对移植静脉再狭窄的影响

目的 观察三七总皂苷(PNS)对大鼠移植静脉再狭窄的影响.方法 建立SD大鼠颈外静脉颈总动脉旁路移植模型,随机分为假手术组、模型组和PNS组,造模后第2天开始灌胃给药,PNS组给予PNS(100 mg/kg),假手术组、模型组灌胃等量蒸馏水(10 ml/kg).给药14 d后,取静脉血管桥固定,观察血管内膜增生,免疫组织化学测定增殖细胞核抗原(PCNA)表达及TUNEL法检测平滑肌细胞凋亡.结果 上述3组的内膜厚度分别为(4.05±0.85)、(26.30±1.15)、(10.80±0.98)μm;内膜/中膜分别为(0.22±0.09)、(0.76±0.27)、(0.45±0.23),PNS组新内膜厚度明显低于模型组(P＜0.05);模型组的PCNA表达量(A值)为(23.6±4.3),明显高于PNS组(11.5±3.6,P＜0.05);模型组的凋亡细胞百分数为(4.3±1.9),明显低于PNS组(20.3±3.5,P＜0.05).结论 PNS可以抑制静脉移植血管桥新生内膜的增生,对预防移植血管再狭窄有一定作用.

Abstract：

Objective To observate the effects of panax notoginseng saponin (PNS) on restenosis of rat vein graft.Methods Jugular vein-to-artery bypass grafting was performed on 30 Sprague-Dawley rats.The rats were divided into three groups: sham group, model group and PNS group.Drugs were administered at the second day after the operation for 14 days.The grafts were harvested for histochemical staining to observe the hyperplasia of neointima, and proliferating cell nuclear antigen (PCNA) expression,and apoptosis of smooth muscle cells were detected by TUNEL.Results In sham group, model group and PNS group, the endometrial thickness was (4.05 ±0.85), (26.30 ± 1.15), ( 10.80 ±0.98) μm; the intima/media was (0.22 0.09), (0.76 0.27), (0.45 0.23), respectively.The neointimal thickness in PNS group was significantly less than in model group ( P ＜ 0.05 ).The PCNA expression in model group (A value) was ( 23.6 ± 4.3 ), significantly higher than in PNS group ( 11.5 ± 3.6 ) ( P ＜ 0.05 ).The percentage of apoptotic cells in model group was (4.3 ± 1.9), significantly lower than in PNS group (20.3 ± 3.5 ) (P ＜ 0.05 ).Conclusion PNS can inhibit the neointimal hyperplais of vein graft, which can prevente restenosis after bypass grafts.     

术前放疗对犬腹主动脉和下腔静脉人工血管置换术后人工血管内膜的影响

目的 观察术前放疗对犬腹主动脉、下腔静脉人工血管置换术后人工血管内膜的影响.方法 杂种犬18只,随机分为放疗组和对照组各9只.放疗组对标记的拟行人工血管移植的血管区行分割放疗,6周后于肾动脉下腹主动脉、下腔静脉行ePTFE人工血管置换术,4周后取标本.对照组除不放疗外各项操作同放疗组.观察两组动物人工血管的通畅率,并行HE染色和免疫组化PCNA和CD34染色.结果 放疗组有2犬术后当天死亡,对照组全部存活.放疗组术后3条静脉人工血管完全堵塞,对照组2条完全堵塞,两者差异无统计学意义(P>0.05).两组动脉人工血管均通畅,内膜完整,但内皮细胞覆盖不完全.放疗组的吻合口近、远端处CD34阳性细胞数差异无统计学意义,而在人工血管中部放疗组低于对照组(P<0.05);放疗组吻合口近、远端及人工血管中部内膜厚度均较对照组薄(P<0.05);而放疗组3个点PCNA阳性细胞表达较对照组为低(P<0.05).结论 术前放疗对人工血管置换术后4周内膜的增生有抑制作用,不会降低其通畅率.     

32 P局部照射对移植静脉内膜平滑肌细胞增殖与凋亡的影响

目的 研究β射线局部照射对自体移植静脉内膜平滑肌细胞（VSMC）增生与凋亡的影响及可能机制。方法 建立80只大鼠自体静脉移植模型,随机分成^32P局部照射组、对照组,每组按3、7、14、28d随机分成4个亚组、每亚组10只。取材固定,弹力纤维染色,增殖细胞核抗原、p53、bcl-2、bax免疫组化测定,TUNEL法检测静脉平滑肌细胞的凋亡,计算机图象分析仪测量移植血管内膜厚度,计算细胞增殖及凋亡百分化。结果 术后2组移植静脉段的内膜平均厚度：7、14、28d,照射组明显 于对照组（t＝15．694,P＜0．05）;7、14d照射组VSMC增殖较对照组受到明显抑制（t＝60．157,P＜0．01）。凋亡指数14d照射组高于对照组（t＝56．176,P＜0．01）。p53的表达,2组间差异无显著性意义（t＝0．473,P＞0．05）,bax与bcl－2的表达,14d照射组高于对照组（t＝9．783,P＜0．05）。结论 ^32P局部照射可以抑制自体移植静脉的内膜增生及VSMC的增殖,促进VSMC的凋亡,可能是通过bax、bcl－2基因的表达实现的。     

伊马替尼抑制大鼠静脉移植物内膜增生

目的 观察伊马替尼对自体移植静脉内膜增生的影响.方法 建立大鼠自体颈外静脉移植模型,实验分为4组:移植组、低剂量给药组、高剂量给药组及对照组.移植4周后取移植静脉,行病理学检查观察内膜增生情况,免疫组织化学及Western blot法检测PDGFRβ、ERK及P-PDGFRβ、P-ERK蛋白表达情况.结果与对照组比较,移植组和低剂量给药组内皮下平滑肌细胞大量增生,静脉内膜显著增厚,管腔明显狭窄,高剂量给药组内膜无明显增厚.Western blot结果显示,移植组血管P-PDGFRβ蛋白含量(P-PDGFRβ/GAPDH)较对照组明显增加(0.81±0.06比0.18±0.02,P<0.05),而高剂量给药组较移植组明显减少(0.32±0.03比0.81±0.06,P<0.05),低剂量给药组与移植组比较差异无统计学意义(P>0.05),P-ERK蛋白表达亦呈同样趋势变化.结论 高剂量伊马替尼能有效抑制自体移植静脉内膜增生,其机制可能与抑制PDGF信号通路蛋白磷酸化,从而抑制平滑肌细胞增殖有关.     

Celiprolol reduces the intimal thickening of autogenous vein grafts via an enhancement of nitric oxide function through an inhibition of superoxide production

BACKGROUND: Beta-adrenoceptor antagonist celiprolol has been widely used as an effective antihypertensive agent. Some studies reported that celiprolol enhances nitric oxide production. The purpose of the present study is to examine the effects of celiprolol on vein graft intimal hyperplasia and endothelium-dependent nitric oxide (NO)-mediated relaxation. METHODS: Japanese white rabbits were randomized to a control group that was fed regular rabbit chow or to a celiprolol group that was fed regular rabbit chow supplemented with 100 mg/body celiprolol sodium. The reversed jugular vein was implanted into the carotid artery. At 2 and 4 weeks after the operation, vein grafts in both groups were harvested, and intimal hyperplasia of the vein grafts was assessed. At 4 weeks after the operation, harvested vein grafts from both the groups were examined on the endothelium-dependent relaxation by application of Ach and were examined to detect for endothelial NO synthase (eNOS) expression and superoxide anion production. RESULTS: Celiprolol inhibited intimal hyperplasia of carotid interposition-reversed jugular vein grafts 4 weeks after implantation (Intima/media index of celiprolol group, 0.48 +/- 0.01 vs control group, 1.07 +/- 0.08, P < .05) and suppressed cell proliferation in the neointima 2 weeks after implantation. In addition, celiprolol significantly enhanced endothelium-dependent NO-mediated relaxation in the vein graft with no change in eNOS expression and a reduction in superoxide production. CONCLUSIONS: These novel findings clearly demonstrate that beta-adrenoceptor antagonist celiprolol can suppress intimal hyperplasia of the vein graft, which may be due to the enhancement of nitric oxide function through an inhibition of superoxide production. These results strongly support the clinical usefulness of celiprolol administration for preventing intimal hyperplasia of the vein graft after bypass grafting.     

Perivenous support reduces early changes in human vein grafts: studies in whole blood perfused human vein segments

BACKGROUND: Patency of vein grafts in coronary artery bypass grafting procedures is generally less favorable than those of selected arterial grafts. However, vein grafts still are needed in cardiac operations. It would be desirable to find measures to improve the patency of vein grafts next to antithrombotic regimens. Animal studies demonstrated that arterial pressure induces overdistention of the thin-walled vein grafts and that prevention of this overdistention with extravascular support ameliorates the arterialization process with, subsequently, more favorable patency. To evaluate whether perivenous stenting of the rather muscular human vein grafts is also beneficial, we designed an in vitro model to study the early effects of perivenous support in human vein grafts. METHODS: Seven paired segments of human vein graft obtained during coronary artery bypass grafting procedures were placed in a perfusion circuit and perfused simultaneously with autologous whole blood, with a pressure of 60 mm Hg (nonpulsatile flow). After 30 minutes of perfusion, one segment, and after 60 minutes of perfusion, the remaining segment were taken for histologic and immunohistochemical examination. In the next experiments 7 segments of human vein graft were placed in the circuit and supported with a polytetrafluoroethylene graft to prevent overdistention with 7 unstented segments as controls. RESULTS: In unsupported vein grafts perfused with autologous blood under a pressure of 60 mm Hg, a complete de-endothelialization was shown after 1 hour of perfusion. In the study vein grafts, with a perivenous polytetrafluoroethylene graft preventing overdistention (n = 7), the endothelium remained intact. Electron microscopic investigation of the media showed severe damage in the circular smooth muscle layer in the unstented group, whereas in the stented group almost no injury was found. CONCLUSION: In our in vitro closed-loop model, reproducible vessel wall changes were observed in all human vein graft specimens studied. The beneficial effect of perivenous support could also be established for the human greater saphenous vein, providing a basis for clinical application.