钙稳态失衡在内皮损伤后血管平滑肌增生中的作用

目的探讨内皮剥脱后血管平滑肌细胞钙稳态的变化及其在内皮损伤诱导血管平滑肌细胞的增殖中的作用。方法在大鼠球囊内皮剥脱模型上，用３Ｈ－胸腺嘧啶核苷和３Ｈ－亮氨酸掺入及４５Ｃａ转运的方法。结果内皮损伤可导致血管平滑肌细胞增殖、内膜增厚；血管平滑肌细胞钙内流增多，剥脱后３天时为４．１２±０．２８、对照组为３；２８±０．１４ｎｍｏｌ／×１０６细胞（Ｐ＜０．０５）；１０天时为４．０９±０．２１、对照组３．３１±０．０９ｎｍｏｌ／×１０６细胞，（Ｐ＜０．０１）、钙外移减少、钙含量升高（剥脱后３天时为９９５±５４、对照组为６９５±３３ｎｍｏｌ／×１０６细胞（Ｐ＜０．０１）；１０天时为１０２２±９４对照组、７０９±３２ｎｍｏｌ／×１０６细胞（Ｐ＜０．０１））、肌浆网和线粒体钙摄取功能增强；应用钙通道阻断剂治疗可以调整内皮剥脱后血管平滑肌细胞的钙稳态失衡，还可以抑制内皮损伤诱导的血管平滑肌细胞增殖。结论钙稳态失衡可能是内皮损伤引起血管平滑肌细胞增殖的细胞学机制之一。     

川芎嗪对血管紧张素Ⅱ诱导的血管平滑肌细胞增殖的抑制作用及机制

目的探讨川芎嗪对血管紧张素Ⅱ诱导的血管平滑肌细胞增殖的影响。方法建立血管紧张素Ⅱ诱导血管平滑肌细胞增殖模型,用酶促反应定磷法观察不同浓度的川芎嗪在不同时段内对血管平滑肌细胞中钙调蛋白和钙调神经磷酸酶活性的影响。结果与正常对照组比较,血管紧张素Ⅱ组能够明显刺激血管平滑肌细胞增殖,血管紧张素Ⅱ处理的血管平滑肌细胞的钙调蛋白和钙调神经磷酸酶活性及细胞增殖活度均较正常对照组显著增高(P<0.01)。同时加川芎嗪处理后,各组钙调蛋白和钙调神经磷酸酶活性均显著下降(P<0.01)。结论川芎嗪对血管紧张素Ⅱ诱导的血管平滑肌细胞增殖有显著抑制作用,其抑制机制可能与其干预钙调神经磷酸酶依赖的信号转导途径有关。     

MAPK介导血管球囊损伤后血管平滑肌细胞的增殖

目的探讨血管球囊损伤后诱导的血管平滑肌细胞增殖的信号传递途径。方法采用同位素技术测定3H-TdR掺入和丝裂素活化蛋白激酶(MAPK)活性。结果 血管球囊损伤后诱导了血管平滑肌细胞增殖,同时有MAPK活性明显增加。结论血管球囊损伤后诱导的血管平滑肌细胞增殖可能是通过增加MAPK活性途径实现的。     

川芎嗪对血管平滑肌细胞增殖及表达c-myc基因的影响

为观察川芎嗪对血管平滑肌细胞增殖的影响,在建立凝血酶诱导的体外培养的兔主动脉血管平滑肌细胞增殖模型后,应用免疫细胞化学方法观察川芎嗪对血管平滑肌细胞表达ｃ－ｍｙｃ基因蛋白的影响;并用流式细胞术观察了血管平滑肌细胞增殖周期的变化。结果发现,川芎嗪能够显著抑制凝血酶诱导的血管平滑肌细胞ｃ－ｍｙｃ基因蛋白表达增加,使血管平滑肌处于ＧＩ期的细胞数显著增多,Ｓ期和Ｇ２＋Ｍ期的细胞数显著减少。结果提示,川芎嗪对凝血酶诱导的血管平滑肌细胞增殖有显著抑制作用,其机制与抑制ｃ－ｍｙｃ基因表达有关。     

牛磺酸对内皮剥脱皮血管平滑肌细胞增生的影响

本实验在整体和细胞水平上观察了牛磺酸对内皮损伤后血管平滑肌细胞（ＶＳＭＣ）增生的影响及机制。结果表明，内皮损伤可导致ＶＳＭＣ增生，使内膜增厚。应用牛磺酸后可抑制内皮损伤诱导的ＶＳＭＣ＾３Ｈ－ＴｄＲ和＾３Ｈ－亮氨酸掺入的增加及内膜增厚，并对内皮损伤诱导的ＶＳＭＣ钙内流增加及细胞钙含量升高有明显的抑制作用。这提示牛磺酸对内皮损伤诱导的ＶＳＭＣ增生有抑制作用，这可能是通过抑制钙内流，降低钙含量实现的。     

苯扎贝特对血小板源生长因子诱导的血管平滑肌细胞增殖和小凹蛋白1表达的影响

目的 观察苯扎贝特对血小板源生长因子诱导的大鼠血管平滑肌细胞增殖及小凹蛋白1表达的影响并探讨其机制.方法 体外植块贴壁法培养大鼠胸主动脉血管平滑肌细胞,噻唑兰比色法检测各组细胞增殖情况,Western Blotting法观察各组小凹蛋白1的表达情况.结果 不同浓度的苯扎贝特对血小板源生长因子诱导的血管平滑肌细胞增殖均有一定的抑制作用,随浓度增加,其抑制作用增强(P<0.01).血小板源生长因子干预组小凹蛋白1的表达较对照组明显降低(P<0.01),而用不同浓度的苯扎贝特干预后小凹蛋白1的表达明显升高(P<0.01),且随着苯扎贝特浓度增加,小凹蛋白1的表述明显增加.结论 苯扎贝特抑制血小板源生长因子诱导的血管平滑肌细胞增殖的同时可以上调小凹蛋白1的表述.     

氟伐他汀对高血压血管平滑肌细胞增殖的影响

目的：探讨氟伐他汀对自发性高血压大鼠血管平滑肌细胞增殖的抑制作用。方法：培养自发性高血压大鼠主动脉血管平滑肌细胞,不同浓度的氟伐他汀和甲羟戊干预后,进行细胞计数和＾３Ｈ－ＴｄＲ掺入率的测定。结果：（１）氟伐他汀呈浓度依赖性（１０＾－５￣１０＾－７ｍｏｌ）抑制血管平滑肌细胞数目的增加和＾３Ｈ－ＴｄＲ的掺入率;（２）１０＾－３ｍｏｌ的甲羟戊酸几科完全逆转了氟伐他汀对血管平滑肌细胞增殖的抑制作用。结论：     

三七总皂甙对血管平滑肌细胞增殖及c-myc基因表达的影响

目的探讨三七总皂甙对血小板源生长因子刺激的血管平滑肌细胞增殖的影响及其可能机制。方法运用血小板源生长因子刺激兔体外血管平滑肌细胞增殖模型,通过四甲基偶氮唑盐比色法、流式细胞术及免疫细胞化学法观察三七总皂甙对其增殖活性、细胞周期及c-myc蛋白表达的影响。结果血小板源生长因子显著刺激血管平滑肌细胞增殖,三七总皂甙呈浓度依赖性抑制血管平滑肌细胞增殖,对血小板源生长因子诱导的血管平滑肌细胞增殖亦具有显著抑制作用;三七总皂甙作用下血管平滑肌细胞处于G1/G0期的细胞数增多,而G2/S期的细胞数显著减少,c-myc蛋白的表达亦降低。结论三七总皂甙对基础状态下及血小板源生长因子诱导的血管平滑肌细胞增殖均具有显著抑制作用,部分机制与其阻滞血管平滑肌细胞G1/G0期向S期转化以及下调c-myc基因表达有关。     

槲皮素对兔球囊血管成形术后管壁增生及培养的动脉平滑肌细胞增殖的影响

目的：观察槲皮素对培养的兔胸主动脉平滑肌细胞增殖及球囊血管成形术后管壁的增生反应。方法：将槲皮素（０．６μｍｏｌ／Ｌ，３．０μｍｏｌ／Ｌ，１５．０μｍｏｌ／Ｌ）加入平滑肌细胞培养液培养后进行细胞计数，并测定氚－胸腺嘧啶脱氧核苷（３Ｈ－ＴｄＲ）放射性强度。应用球囊损伤动脉内膜加高脂饲养的方法建立髂动脉粥样硬化模型，对２０只模型兔进行球囊血管成形术。其中１０只于术前３天起至术后４周持续腹腔注射槲皮素２００ｍｇ／ｋｇ，每日１次。另１０只为对照组。结果：槲皮素能抑制胸主动脉平滑肌细胞的增殖及３Ｈ－ＴｄＲ的摄取（与对照组相比Ｐ＜０．０５或０．０１）；增加球囊血管成形术后血管腔面积，减少内膜和中膜厚度（与对照组相比Ｐ＜０．０５）。结论：槲皮素能抑制动脉平滑肌细胞增殖，预防血管再狭窄；槲皮素对酪氨酸蛋白激酶的抑制作用可能是其主要机制之一。     

HMG-CoA还原酶抑制剂对自发性高血压大鼠血管平滑肌细胞增殖的作用

探讨羟甲基戊二酰辅酶A还原酶抑制剂对自发性高血压大鼠血管平滑肌细胞增殖的抑制作用及其机制。培养自发性高血压大鼠主动脉血管平滑肌细胞,应用不同浓度HMG－CoA还原酶抑制剂洛伐他汀,辛伐他汀和氟伐他汀及血管紧张素Ⅱ,甲羟戊酸等干预后,进行细胞计数和^3H-TdR掺入率测定。结果发现,洛伐他汀,辛伐他汀和氟伐他汀均呈浓度依赖性抑制小牛血清和血管紧张素Ⅱ诱导的血管平滑肌细胞数和^3H-TdR掺入率增加;但以氟伐他汀的抑制作用最大,辛伐他汀次之,洛伐他汀最小,10^-3mol/L甲羟戊酸几乎完全逆转洛伐他汀,辛伐他汀和氟伐他汀对血管平滑肌细胞增殖的抑制作用。提示此3种HMG－CoA还原酶抑制剂均能高血压大鼠血管平滑肌细胞增殖,但作用并不完全相同;甲羟戊酸代谢途径可能参与血管平滑肌细胞增殖过程。     

缬沙坦对血管损伤小鼠血管重构的影响

目的观察缬沙坦对血管损伤小鼠血管壁内膜、中膜的影响。方法8周龄雄性C57BL／6野生型小鼠80只,随机分为手术组（n=20）、治疗组（n=20）、假手术组（n=20）和对照组（n=20）。手术组：行聚乙烯套管包裹股动脉手术,术后开始蒸馏水灌胃治疗（1mL／次,qd）;治疗组：行聚乙烯套管包裹股动脉手术,术后开始缬沙坦灌胃治疗（10mg／kg,qd）;假手术组：游离出股动脉不套管,术后不灌胃;对照组：不手术,不灌胃。于手术后第14天处死小鼠,取各组损伤套管处股动脉（对照组取相应部位股动脉）;采用苏木素-伊红（HE）染色,光镜下观察血管形态学变化,NIH分析软件测量新生血管内膜和中膜的面积。结果各组中膜均无增厚表现,与术前相比差异无统计学意义（P〉0．05）。假手术组及对照组无新生内膜增厚,与实验前相比差异无统计学意义（P〉0．05）;手术组与治疗组内膜均增厚、面积增大,其中手术组内膜面积增厚程度最大,但与治疗组相比差异无统计学意义（P〉0．05）。手术组与假手术组及对照组相比,内膜面积比较差异统计学意义（P〈0．05）。结论短期应用缬沙坦能一定程度上抑制损伤后血管内膜增厚、抑制血管重构。     

Early experience on peripheral vascular application of the vascular plugs

BackgroundTranscatheter closure of various congenital and acquired vascular malformations with Amplatzer Vascular plugs I and II has been established. Here we present our experience with device closure.Materials and methodsBetween October 2006 and August 2012, nine (three males and six females) patients aged between 11 months and 62 years (mean age 19 years) underwent percutaneous device closure with AVP I and II vascular plugs for congenital and acquired arteriovenous malformation and cardiac diverticulum are presented here.ResultsOne case of coronary cameral fistula, four cases of pulmonary arteriovenous fistula, one case of large major aortopulmonary collaterals (in tetralogy of Fallot closed before intracardiac repair), one case of congenital cardiac diverticulum, one case of fistula between external carotid artery and internal jugular vein and one case of iatrogenic carotid jugular fistula were successfully closed with AVP I and II plugs. Overall in nine cases, 16 AVP I and II plugs were deployed to occlude feeding vessels and one cardiac diverticulum. The technical success rate was 100%. No major complications were observed.ConclusionAmplatzer vascular plugs can be used successfully for closure of various congenital and acquired vascular malformations with good result.     

Intussusceptive angiogenesis and its role in vascular morphogenesis, patterning, and remodeling

New blood vessels arise initially as blood islands in the process known as vasculogenesis or as new capillary segments produced through angiogenesis. Angiogenesis itself encompasses two broad processes, namely sprouting (SA) and intussusceptive (IA) angiogenesis. Primordial capillary plexuses expand through both SA and IA, but subsequent growth and remodeling are achieved through IA. The latter process proceeds through transluminal tissue pillar formation and subsequent vascular splitting, and the direction taken by the pillars delineates IA into overt phases, namely: intussusceptive microvascular growth, intussusceptive arborization, and intussusceptive branching remodeling. Intussusceptive microvascular growth circumscribes the process of initiation of pillar formation and their subsequent expansion with the result that the capillary surface area is greatly enhanced. In contrast, intussusceptive arborization entails formation of serried pillars that remodel the disorganized vascular meshwork into the typical tree-like arrangement. Optimization of local vascular branching geometry occurs through intussusceptive branching remodeling so that the vasculature is remodeled to meet the local demand. In addition, IA is important in creation of the local organ-specific angioarchitecture. While hemodynamic forces have proven direct effects on IA, with increase in blood flow resulting in initiation of pillars, the preponderant mechanisms are unclear. Molecular control of IA has so far not been unequivocally elucidated but interplay among several factors is probably involved. Future investigations are strongly encouraged to focus on interactions among angiogenic growth factors, angiopoetins, and related receptors.     

主髂动脉闭塞手术方式的选择

目的 :探讨腹主动脉下段及髂动脉闭塞手术方式的选择。方法 :对我院 1996年 3月至 2 0 0 2年 1月 4 8例主髂动脉闭塞病例进行回顾性总结。结果 :行主 髂 (股 )动脉人工血管转流术 15例 ,髂 股动脉人工血管转流术 10例。髂动脉内膜剥脱术 1例 ,股 -股动脉人工血管转流术 10例 ,腋 -股动脉人工血管转流术 12例。均得到随访。总有效率 95 8% ,围手术期死亡率 4 17%。人工血管通畅率81 2 %。结论 :解剖途径人工血管转流术是治疗本病的首选方法 ,以获得较高的通畅率。对于高龄、体弱者 ,特别是全身一般情况差 ,合并高血压、糖尿病、冠心病、肺气肿等慢性病的患者 ,应采用解剖外途径人工血管转流术 ,以减低手术死亡率     

Effects of Estrogen Level on the Function of Vascular Endothelial Cells and Expression of Vascular Cell Adhesion Molecule-1(?)

Objectives To ob-serve the effect of different estrogen levels on the secretory function of vascular endothelial cells of female rats, and study the effect of modulation of estrogen level on the expression of vascular cell adhesion molecule - 1 and the concentration of estrogen receptor in vascular endothelial cells. Methods Radioim-munology was used to measure the serum concentration of endothelin and PGI2, and copper - cadmium reduction was employed to measure the serum content of nitrogen monoxide. Radioligand binding and flowcy-tometry were used to measure the expression of estrogen receptor and vascular cell adhesion molecule (VCAM - 1) of vascular endothelial cells respectively. Results 1. The serum concentration of nitric oxide and PGI2 decreased when the ovaries of female rats were removed. In ovariectomized rats, given estrogen, the concentration rose ( P < 0. 05), but the plasma concentration of endothelin was adverse to it. 2. The concentration of estrogen receptor of vascular endothelial cel     

高频超声检测脑梗死与短暂性脑缺血发作患者血管内皮功能的探讨

目的:研究脑梗死、短暂性脑缺血发作(TIA)患者颈动脉内-中膜厚度、血管弹性与肱动脉血管内皮功能.方法:研究对象分为3组:脑梗死患者、TIA患者、正常同龄人,每组各30例.用高频超声测量颈动脉内-中膜厚度、收缩期颈动脉内径(DS)、舒张期颈动脉内径(DD),计算颈总动脉壁弹性的相关参数:可扩张度(DC)、顺应性(CC)...     

Structural stability of neoangiogenic intramyocardial microvessels supports functional recovery in chronic ischemic myocardium

We hypothesize that combining angiopoietin-1 (ANG-1) or ANG-2 with vascular endothelial growth factor (VEGF) improves myocardial perfusion and contractile function by modulating vascular adaptation of neoangiogenic microvessels in a chronic ischemic swine model. Four weeks after occlusion of the left circumflex coronary artery (LCx), animals were injected with AdVEGF₁₆₅ (n = 6), AdVEGF₁₆₅+AdANG-1 (n = 6), AdVEGF₁₆₅+AdANG-2 (n = 6) or control vector (n = 5) into the left ventricular posterolateral wall. Regional perfusion by fluorescent microspheres and segmental myocardial tissue velocity by tissue Doppler imaging (TDI) were assessed at baseline, 4 weeks post occlusion and 4 weeks post therapy. Despite similar vascular growth following VEGF+ANG-1 and VEGF+ANG-2 treatments, transmural myocardial contractility improved only when VEGF was paired with ANG-1. In contrast, regional systolic function deteriorated uniformly across subepicardial, mid-myocardial and subendocardial segments in VEGF and VEGF+ANG-2 treated groups. Contractile improvement was associated with enhanced vascular stability through augmented arteriole formation, tight structural integration between VE-cadherin and β-catenin at endothelial junctions and improved cross-talk between endothelium and myocardium. Structural stability of developing intramyocardial microvessels contributes to systolic function during ischemic neovascularization. Coordinated regulation of angiogenic revascularization that supports vascular stability is a key aspect in improving therapeutic outcomes in ischemic myocardium.     

干细胞分化为平滑肌细胞参与血管病变

动脉粥样硬化,冠状动脉介入术后再狭窄以及器官移植相关的血管病变,以增生内膜平滑肌细胞增殖,分泌细胞外基质为主要特点。传统观点认为增生内膜的平滑肌细胞系血管中层平滑肌细胞向内膜迁移,增殖的结果。现代认为干细胞能分化为血管平滑肌细胞,参与上述疾病的发生、发展。     

辛伐他汀对血管平滑肌细胞增殖和迁移的影响

目的观察辛伐他汀对血管平滑肌细胞增殖、迁移及血管内皮生长因子表达的影响。方法体外培养大鼠原代血管平滑肌细胞,体内建立大鼠动脉粥样硬化血管损伤模型,分为正常对照组、动脉粥样硬化损伤组、低剂量和高剂量辛伐他汀组。4周后处死动物,酶法测定血脂水平,检测胸主动脉和左颈总动脉内膜/(内膜 中膜)比值,免疫组织化学和逆转录聚合酶链反应法检测血管内皮生长因子的表达。结果辛伐他汀对血管平滑肌细胞的增殖和迁移无双向调节作用。小剂量辛伐他汀对血管平滑肌细胞的增殖和迁移无促进作用,大剂量辛伐他汀抑制血管平滑肌细胞的增殖和迁移,且随着时间延长和浓度增加其抑制作用增强,这种作用不依赖辛伐他汀的调脂性。辛伐他汀能减少血管平滑肌细胞血管内皮生长因子的表达,且高浓度的辛伐他汀显著减少血管内皮生长因子的表达。结论辛伐他汀可能通过减少血管平滑肌细胞血管内皮生长因子的表达来抑制血管平滑肌细胞的增殖和迁移。