早期原发性高血压患者血管内皮功能研究

[目的]观察早期原发性高血压患者肱动脉内皮功能状态和血管活性物质的变化。[方法]对40例早期原发性高血压患者(早期高血压组)和40例健康对照者(对照组),以高分辨率超声测定肱动脉血流介导内皮依赖性舒张功能(FMD),并检测血一氧化氮(NO)、降钙素基因相关肽(CGRP)、血浆内皮素(ET-1)、假性血管性血友病因子(VWF)的变化。[结果]早期原发性高血压组的FMD和NO、CGRP降低,ET-1、VWF升高,与健康对照组相比差异有统计学意义(P﹤0.05)。血NO水平变化与FMD的变化一致(r=0.511,P﹤0.01)。[结论]原发性高血压患者在早期已发生肱动脉内皮依赖性舒张功能降低,与NO水平下降有关。     

不同剂量阿托伐他汀对急性冠状动脉综合征患者动脉内皮依赖性舒张功能影响的研究

目的探讨不同剂量的阿托伐他汀对急性冠状动脉综合征(ACS)患者肱动脉内皮依赖性舒张功能(FMD)的影响。方法102例ACS患者随机分为阿托伐他汀40 mg组和10mg组,测定治疗前和1周后肱动脉内皮依赖性舒张功能;同时选择健康的体检者30例作为正常对照组。结果ACS患者由血流介导的肱动脉内皮依赖性舒张功能明显低于正常对照组(P<0.01),阿托伐他汀40 mg组和10 mg组治疗前和治疗后1周后各项血脂水平差异无统计学意义(P>0.05)。阿托伐他汀40 mg组治疗1周后FMD明显改善(P<0.01),阿托伐他汀10 mg组治疗1周后FMD有改善,但差异无统计学意义(P>0.05)。结论短期大剂量的阿托伐他汀直接改善肱动脉内皮依赖性舒张功能,阿托伐他汀改善FMD的作用独立于其调血脂作用之外。     

高频超声对甲状腺功能减低患者血管内皮依赖性舒张功能的诊断价值

目的：了解高频超声在检测甲状腺功能减低患者血管内皮依赖性舒张功能中的价值。方法：用高频超声对82例甲状腺功能减低患者（甲减组）及90例无高血压病、糖尿病及心脑血管疾病的志愿者（对照组）检查血管内皮依赖性舒张功能,测定两组患者肱动脉内皮依赖性舒张功能并进行对照分析。结果：甲状腺功能减低患者反应性充血诱发的肱动脉内径百分变化率明显低于对照组（P〈0.01）。结论：甲状腺功能减低患者存在内皮依赖性舒张功能障碍,高频超声对评价血管内皮依赖性舒张功能有重要价值。     

氯沙坦改善高血压患者血管内皮功能的探讨

目的探讨氯沙坦改善高血压患者中内皮功能的作用.方法120例Ⅰ期高血压病患者随机分成两组,每组60例.分别进行12w的氯沙坦(Losartan 50mg每天一次)和氢氯噻嗪(HCT 25mg每天两次)治疗.观察两组病人的血压及内皮功能的变化.结果两组药物治疗后比治疗前血压有下降(P＜0.05),降幅相等.氯沙坦组治疗后血流介导的肱动脉扩张率(FMD)增加,肱动脉血流速度增快,6-K-PGF1α、NO增加,ET-1降低(P均＜0.05),而氢氯噻嗪组无此变化.两组的非内皮依赖性肱动脉舒张(NTG-MD)治疗前后均无明显差异(P＞0.05).结论氯沙坦可改善Ⅰ期高血压病患者血管内皮作用,可能产生良好的远期效应.     

糖尿病并发冠心病超声检测颈动脉粥样硬化及内皮功能临床分析

目的 探讨糖尿病并发冠心病患者的动脉粥样硬化及内皮功能变化.方法 采用二维超声测定颈动脉内中膜厚度和硬化斑块指数衡量动脉粥样硬化程度,测定肱动脉内径代表血管内皮舒张功能.患病组36例,对照组40例.结果 患病组,IMT、动脉粥样硬化斑块检出率、硬化斑块指数(Plaque index,PI)明显大于对照组(P＜0.05).患病组与对照组相比,肱动脉内皮依赖性血管舒张功能明显受损(P＜0.01),内皮非依赖性舒张功能则无明显变化(P》0.05).结论 糖尿病并发冠心病患者存在严重颈动脉粥样硬化及内皮依赖性血管舒张功能明显受损.     

高血压及高血压合并糖尿病患者内皮功能的研究——附55例报告

[目的]评估高血压及高血压合并糖尿病患者的血管内皮功能。[方法]将30例单纯高血压患者设为A组,25例高血压合并2型糖尿病患者设为B组,另设同期门诊体检血压、血糖正常的30名健康者为C组。3组均采用彩色多普勒超声检测肱动脉血管内皮的血流介导的舒张功能(flow-mediated dilation,FMD),同时观察3组的血压、血脂、空腹血糖水平,并对FMD的影响因素作相关分析。[结果]①A组和B组的收缩压与舒张压均高于C组(P﹤0.05～0.01);②A组和B组的甘油三酯水平均高于C组,B组的空腹血糖高于其他2组(P﹤0.05～0.01);③A组和B组的FMD较C组明显降低,而B组较A组降低幅度更为明显(P﹤0.05～0.01);④单因素相关分析结果显示,FMD与收缩压、舒张压、空腹血糖呈负相关(r分别为-0.635、-0.255、-0.535,P﹤0.05～0.01),与甘油三酯、胆固醇无相关关系;多因素分析结果显示,仅收缩压被引入回归方程(R2=0.388,P﹤0.01)。[结论]高血压可造成血管内皮功能受损,如合并糖尿病则血管内皮功能损害进一步加重。     

卡托普利对高血压病患者内皮功能和非对称二甲基精氨酸的影响

目的 观察高血压病患者服用卡托普利后肱动脉内皮功能和血浆ADMA的变化.方法 入选35例高血压病患者口服卡托普利25 mg 3次/d,随访3月(高血压组),同时选择32例健康成人作为对照组,观察对照组和高血压病患者治疗前后肱动脉基础内径、充血后内径的变化以及采用HPLC法检测血浆非对称二甲基精氨酸(ADMA)的变化,并观察患者血压变化和药物的不良反应.结果 高血压病患者血压较对照组明显升高(P＜0.05).同对照组相比,高血压病患者肱动脉血流介导的血管舒张功能(FDM)显著降低(5.84±4.72 vs 12.7±3.47%,P＜0.05),血浆ADMA水平显著增加(0.87±0.35vs 0.58±0.36μmol/L,P＜0.05).经卡托普利治疗3月后,高血压病患者的血压下降,肱动脉FDM好转(9.75±3.28 vs 5.84±4.72%,P＜0.01),血浆ADMA水平降低(0.65±0.31 vs 0.87±0.35,μmol/L,P＜0.01).结论 卡托普利不仅可降低高血压病患者血压,同时可显著改善患者的内皮功能.     

肱动脉内皮功能及颈动脉内中膜厚度与高血压、糖尿病的关系

[目的]探讨肱动脉血管内皮功能及颈动脉内-中膜厚度(intima-media thickness,IMT)与高血压和糖尿病的关系. [方法]选择原发性高血压41例(A组)、2型糖尿病31例(B组)和健康对照组29例(C组),利用高频彩色多谱勒超声测检测颈动脉IMT,在静息、反应性充血和舌下含服硝酸甘油后用检测肱动脉内径的变化. [结果]静息状态下肱动脉内径3组间无统计学差异(P＞0.05);A组和B组肱动脉血流介导的血管扩张(FMD)与C组比较均有统计学差异(P＜0.01);B组含服硝酸甘油后肱动脉内径的扩张(NID)与A组及C组比较有统计学差异(P＜0.05),A组与C组比较无统计学差异(P＞0.05).A、B组的颈动脉IMT与C组比较有统计学差异(P＜0.05),但60岁以后3组间无统计学差异(P＞0.05). [结论]肱动脉内皮功能和颈动脉IMT与高血压和糖尿病密切相关,肱动脉内皮功能损伤较颈动脉IMT异常出现早.采用多普勒超声技术联合检测肱动脉皮功能和颈动脉厚度是评价血管内皮细胞功能异常的有效方法.     

老年高血压患者血管弹性、内皮功能、虚弱指数的研究

目的探究老年高血压患者的血管弹性状态、内皮功能、虚弱指数的研究。方法选取承德医学院附属医院2017年2月～2018年2月收治并进行血管相关功能检测的老年高血压患者50例(高血压组),同期住院进行健康体检者50例作为健康对照组,通过肱动脉二维超声显像,并测定肱动脉内径及反应性充血变化。结果反应性充血引起肱动脉内径的变化在高血压组减弱,高血压组的反应性充血舒张百分比较对照组低,比较差异有显著统计学意义(P 0.01)。老年高血压患者的非内皮依赖性血管扩张能指标与健康对照组比较差异无统计学意义(P 0.05);内皮依赖性血管扩张功能指标明显低于健康对照组,差异有统计学意义(P 0.01)。高血压组患者由于高血压、饮食、服药及年龄的原因造成了身体不健康指数的增高,其虚弱指数显著高于健康对照组,差异有统计学意义(P 0.01)。结论老年高血压患者的血管弹性状态和内皮功能受高血压影响,由于疾病相关因素导致虚弱指数上升,应在临床诊断治疗中予以关注。     

海洛因对人体血管内皮舒张功能影响的临床研究

目的研究静脉注射和非静脉注射吸食海洛因患者肱动脉血管内皮舒张功能的改变,探讨海洛因对人体神经一内分泌一免疫功能的影响及其相互之间的关系。方法超声检查34例静脉注射海洛因患者、30例非静脉注射海洛因患者和30例正常人对照组,肱动脉内皮依赖性（EDD）及非内皮依赖性（EID）舒张功能,并进行对比分析。结果三组肱动脉内径基础值无统计学意义（P〉0．05）;静脉注射海洛因患者肱动脉内皮依赖性和非内皮依赖性舒张功能,EDD／EID与对照组比较有显著差异（P〈0．01）;非静脉注射海洛因患者肱动脉内皮依赖性和非内皮依赖性舒张功能,EDD／EID与对照组比较有差异（P〈0．05）。结论静脉注射和非静脉注射海洛因患者肱动脉内皮依赖性和非内皮依赖性舒张功能明显受损。肱动脉血管内皮舒张功能检查为吸食海洛因患者神经一内分泌一免疫功能损伤提供依据,还可以作为监测和评估病情的指标。     

Thioredoxin reductase regulates angiogenesis by increasing endothelial cell-derived vascular endothelial growth factor

Low selenium (Se) status increases angiogenesis by inducing the production of vascular endothelial growth factor (VEGF); however, the mechanism responsible for VEGF up-regulation has yet to be characterized. Se's ability to control cellular oxidative state through its incorporation into selenoproteins such as thioredoxin reductase (TrxR) may explain previous studies that connect Se status to tumor angiogenesis. Therefore, the focus of this study was to determine if altered VEGF expression and angiogenesis due to decreased Se levels are influenced by reduced TrxR activity. We found that chemical inhibition of TrxR in Se-sufficient endothelial cells (ECs) was associated with increases in VEGF and VEGF receptor expression, cell migration, proliferation, and angiogenesis to levels similar to those seen in Se-deficient ECs. Specific inhibition of glutathione peroxidase did not affect pro-angiogenic responses, indicating a unique role of the TrxR system during low Se status. These data correlate changes in TrxR activity with changes in VEGF expression and angiogenic development in ECs, which is significant because minimal mechanistic data exist that explain the role of Se in cancer prevention. Understanding the importance of the tumor microenvironment in contributing to angiogenic regulation has the potential to significantly impact breast cancer chemoprevention strategies by focusing on maintaining proper EC function within the mammary gland.     

精氨酸-甘氨酸-天冬氨酸肽对血管内皮细胞生长因子分泌的影响

目的研究精氨酸-甘氨酸-天冬氨酸肽(RGD肽)对血管内皮细胞(VEC)分泌血管内皮细胞生长因子(VEGF)的影响及机制。方法以培养的人大网膜VEC为模型,检测不同浓度RGD肽作用下VEGF浓度及蛋白激酶C(PKC)活性。结果100～300mg/mlRGD肽作用24h后,VEGF浓度及PKC活性较对照组明显升高(P0.01)。结论RGD肽呈浓度依赖性刺激VEC分泌VEGF,PKC介导了RGD肽刺激VEC分泌VEGF的作用。     

增龄对大鼠内皮功能影响的探讨

目的 观察增龄对大鼠血管结构和内皮功能的影响,探讨增龄所致的血管内皮功能障碍的可能机制,为进一步研究如何延缓增龄性内皮功能障碍提供新思路,也为临床提供实验依据.方法 选择青年组(3月龄)、成年组(9月龄)、中年组(15月龄)健康雄性大鼠,通过检测血管内皮功能相关指标(血浆NO、eNOS、iNOS、ET-1及主动脉组织NO、eNOS、iNOS),测定离体主动脉环内皮依赖性与非内皮依赖性血管舒张功能,观察大鼠主动脉的形态学变化,寻找出早期出现内皮功能明显改变的月龄组大鼠.结果 青年组、成年组、中年组大鼠血浆NO、eNOS、iNOS及主动脉组织的NOS活性随月龄增加逐渐降低(P＜0.05);ET-1则逐渐升高(P＜0.05);主动脉环对于乙酰胆碱所致的最大血管舒张程度随着月龄增加降低(P＜0.05),对硝普钠所致的舒张反应各组基本一致(P＞0.05);主动脉形态随着月龄的增加,内膜中膜厚度(T)、内径(D)、内膜中膜厚度/内径(T/D)逐渐增大(P＜0.05);分组回归分析,NO、eNOS、iNOS、ET-1在成年组斜率最大,同其它组比较差异均有统计学意义(P＜0.05),提示此月龄组出现了血管内皮功能明显改变;T、D在中年组斜率最大,同其它组比较差异均有统计学意义(P＜0.05),表明增龄性血管结构改变此期明显,血管功能的改变早于结构的变化.结论 伴随增龄血管内皮功能障碍形成,成年组大鼠是早期出现内皮功能明显改变的月龄组,内皮依赖性血管舒张功能下降,血管功能的改变早于结构的变化.     

GPER介导血管内皮细胞增殖与迁移作用

目的通过观察G蛋白偶联雌激素受体（GPER）激活在血管内皮细胞中的促增殖作用,探讨其在心血管和肿瘤疾病中的可能作用机制。方法使用免疫荧光检测GPER在血管内皮细胞中的表达。采用GPER特异性激动剂G1（10nM）和阻断剂G15（1uM）以及ERK信号阻断剂PD98059（1uM）干预血管内皮细胞,用细胞增殖试剂盒、cck-8试剂盒、Hanging Cell Culture Inserts小室测定G1对内皮细胞增殖以及迁移的作用。结果GPER在牛主动脉内皮细胞中有所表达,GPER的激活对内皮细胞的增殖、活性和迁移有明显的促进作用（P〈0．05）,在G15和PD98059作用下这种促增殖作用消失（P〈0．05）。结论GPER通过ERK1／2信号通路介导血管内皮细胞增殖和迁移作用。     

循环内皮祖细胞及其应用

内皮祖细胞(endothelial progenitor cells,EPCs)是一类能增殖、迁移并分化为成熟血管内皮细胞,但尚未表达成熟血管内皮细胞表型,也未形成血管的前体细胞。对于存在于人体外周血循环中的内皮祖细胞,称为循环内皮祖细胞(circulating endothelial progenitor cells,CEPCs),其参与出生后血管新生和内皮损伤后的修复过程。CEPCs已成为心血管疾病等存在内皮损伤相关研究的热点。本文综述了循环内皮祖细胞的生物学特性,影响循环内皮祖细胞数量和功能的因素,以及循环内皮祖细胞在实际中应用的最新研究进展,为心血管疾病诊断和治疗提供新思路、新手段。     

Oxysterol-induced endothelial cell dysfunction in culture.

Cholesterol oxidation products (oxysterols), such as cholestan-3 beta,5 alpha,6 beta-triol (Triol), may be atherogenic by altering the barrier function of the vascular endothelium. We have shown that incubation of endothelial cell monolayers with Triol increased transendothelial albumin transfer (i.e., decreased barrier function) in a concentration- and time-dependent manner. Such dysfunction of endothelium could result from alterations in membrane characteristics, including changes in membrane-associated enzyme activities. To test this hypothesis, endothelial monolayers were treated with 20 microM Triol and the activities of selected membrane enzymes were measured at 0, 2, 4, 6, 12 and 24 hours. Calcium-adenosine triphosphatase (Ca(++)-ATPase) and sodium, potassium, magnesium-adenosine triphosphatase (Na+, K+, Mg(++)-ATPase) activities were significantly increased after 4 or 2 hours incubation with 20 microM Triol, respectively. 5'-nucleotidase activity was significantly elevated only after a 24-hour exposure to Triol, whereas there was no change in angiotensin-converting enzyme (ACE) activity in response to 20 microM Triol treatment at any time studied. Compared with all concentrations tested 40 microM Triol increased Ca(++)-ATPase activity most markedly, with a significant increase already after a 2-hour exposure. No major morphological changes were noted until 12 hours of exposure to 20 microM Triol; obvious cellular damage was observed by 24 hours. Cultures treated with Triol for 24 hours showed significant signs of toxicity, measured by an elevated [3H]adenine release, compared with control cultures. These data demonstrate that Triol alters the activity of certain membrane-bound enzymes, particularly Na+, K+, Mg(++)-ATPase and Ca(++)-ATPase.(ABSTRACT TRUNCATED AT 250 WORDS)     

Instrumental methods for evaluation of endothelial function

Endothelial dysfunction is a systemic disorder with a key role in the pathogenesis of atherosclerosis and its complications. Current evidence suggests that endothelial status is not determined solely by the individual risk factor burden but is rather regarded as an integrated index of all atherogenic and atheroprotective factors present in an individual, including known as well as yet-unknown variables and genetic predisposition. Endothelial dysfunction reflects a vascular phenotype prone to atherogenesis and may therefore serve as a marker of the inherent atherosclerotic risk in an individual. Recent advances in the understanding of pathophysiology of early atherosclerosis have opened up new opportunities for development of methods for assessment of the earliest changes in the vessel wall. During the last decade some noninvasive techniques have been introduced in clinical practice among which the ultrasound assessment of flow-mediated vasodilation of the brachial artery is the most widely used. These stimuli induce the endothelium to release nitric oxide which causes vasodilation that can be visualized and measured as an index of the vasomotor activity. This technique is attractive because it is non-invasive, accessible and reproducible in everyday clinical practice.