依达拉奉对脑缺血再灌注大鼠血管细胞黏附分子1的影响

目的探讨依达拉奉对脑缺血再灌注大鼠脑组织和血清血管细胞黏附分子1(VCAM-1)和细胞间黏附分子1(ICAM-1)水平的影响。方法将30只雄性SD小鼠随机分为假手术组、缺血再灌注组和依达拉奉组,每组10只。建立大鼠大脑中动脉缺血再灌注模型,24h后采集脑组织和血清,分别采用免疫组织化学、ELISA法检测VCAM-1和ICAM-1水平。结果与假手术组比较,缺血再灌注组大鼠脑组织和血清ICAM-1、VCAM-1明显升高(P<0.05);与缺血再灌注组比较,依达拉奉组脑组织ICAM-1、VCAM-1[(0.14±0.02)μg/L vs(0.19±0.04)μg/L、(0.12±0.02)μg/L vs(0.17±0.03)μg/L,P<0.05]和血清ICAM-1、VCAM-1[(1.03±0.29)μg/L vs(1.29±0.44)μg/L、(170.79±43.42)μg/L vs(261.85±73.05)μg/L,P<0.05]明显降低。结论依达拉奉能改善脑缺血再灌注大鼠的症状,其作用机制之一是抑制ICAM-1和VCAM-1的生成。     

冠心病中医辨证分型与细胞黏附分子的关系

目的检测冠心病(CHD)各证型血清细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1),探讨细胞黏附分子与CHD辨证分型的关系。方法用酶联免疫吸附法(ELISA)检测68例CHD病人(心血瘀阻证25例,痰浊阻脉证22例,虚证21例)和20名健康对照者血清ICAM-1、VCAM-1水平,并比较各指标水平在不同中医证型中的高低。结果血清ICAM-1水平在心血瘀阻证组(234.42ng/mL±84.72ng/mL)、痰浊阻脉证组(218.61ng/mL±59.31ng/mL)明显高于虚证组(133.29ng/mL±44.67ng/mL)和对照组(104.64ng/mL±40.59ng/mL,P<0.01或P<0.05);血清VCAM-1水平心血瘀阻证组(427.68ng/mL±182.74ng/mL)明显高于对照组(304.67ng/mL±180.46ng/mL,P<0.05)。结论不同CHD证型与血清ICAM-1、VCAM-1水平有关。     

蜂胶水提物预处理对血管内皮细胞的保护作用

目的观察蜂胶水提物对损伤血管内皮细胞的保护作用,探讨蜂胶抗动脉粥样硬化的作用及其机制。方法用50 μg/L TNF-α诱导体外培养脐静脉内皮细胞损伤,用50、100、200 mg/L蜂胶水提物分别干预6、12、24 h,分为对照组、模型组、蜂胶低浓度组、蜂胶中浓度组、蜂胶高浓度组、氟伐他汀钠组、联合组,采用流式细胞仪检测细胞间黏附分子1(ICAM-1)和血管细胞黏附分子1(VCAM-1)的表达。结果与对照组比较,模型组ICAM-1和VCAM-1表达明显升高;与模型组比较,蜂胶低浓度组、蜂胶中浓度组和蜂胶高浓度组ICAM-1和VCAM-1明显降低(P0.01)。12 h时与氟伐他汀钠组比较,联合组ICAM-1和VCAM-1表达明显降低(P0.01)。结论蜂胶水提物能降低ICAM-1和VCAM-1的表达。与氟伐他汀钠联合应用,对血管内皮细胞损伤有协同保护作用。     

心力衰竭患者血清胱抑素-C、血管细胞间黏附分子-1和细胞间黏附分子-1水平的表达及意义

目的观察心力衰竭患者血清胱抑素(Cys)-C、血管细胞间黏附分子(VCAM)-1、细胞间黏附分子(ICAM)-1的水平及意义。方法确诊为心力衰竭患者58例作为观察组,25例经体检证实为无明显器质性病变的成人血清标本作为对照组。检测两组血清中Cys-C、VCAM-1和ICAM-1的表达。结果观察组血清中Cys-C、VCAM-1和ICAM-1的表达明显高于对照组(均P<0.05),观察组血清中Cys-C、VCAM-1和ICAM-1的表达与心力衰竭的分级相关,相关性分析显示VCAM-1和ICAM-1呈正相关,其他指标间未见明显相关性。结论心力衰竭患者血清中Cys-C、VCAM-1和ICAM-1高表达对病变的发生和进展有一定的促进作用;VCAM-1和ICAM-1有协同作用。     

瑞舒伐他汀与胃饥饿素对糖脂代谢异常大鼠作用比较

目的观察瑞舒伐他汀与胃饥饿素对糖脂代谢异常模型大鼠血糖、血脂、体质量及血管内皮细胞间黏附分子1(ICAM-1)、血管细胞黏附分子1(VCAM-1)的作用。方法选择健康雄性无特定病原体级Wistar大鼠40只,高脂饮食20d,随机取10只作为对照组,其余大鼠链脲佐菌素诱导糖尿病,造模成功后,随机分为3组,模型组、瑞舒伐他汀组、胃饥饿素组,每组10只。各组大鼠继续给予高脂饮食12周后检测血脂、血糖、体质量和高敏C反应蛋白(hs-CRP)水平,Western blot法检测血管内皮组织中ICAM-1、VCAM-1蛋白表达。结果与对照组比较,模型组体质量、血糖、LDL-C、TC、hs-CRP、ICAM-1、VCAM-1明显增加,瑞舒伐他汀组体质量、血糖、LDL-C、hs-CRP、ICAM-1、VCAM-1明显增加,胃饥饿素组血糖、LDL-C、ICAM-1、VCAM-1明显增加(P0.05,P0.01)。与瑞舒伐他汀组比较,胃饥饿素组血糖、体质量明显降低[(9.89±6.32)mmol/L vs(17.56±3.56)mmol/L,(289.62±32.66)g vs(358.72±30.89)g,P0.01]。结论胃饥饿素不仅调脂、抗炎作用与瑞舒伐他汀相似,而且降糖、降体质量作用优于瑞舒伐他汀。     

慢性阻塞性肺疾病患者血清基质金属蛋白酶及其抑制因子与细胞黏附因子和血管内皮黏附因子的关系研究

目的探讨慢性阻塞性肺疾病(COPD)患者血清基质金属蛋白酶-9(MMP-9)及其抑制因子(TIMP-1)的变化与细胞黏附因子-1(ICAM-1)、血管内皮黏附因子-1(VCAM-1)之间的关系。方法应用酶联免疫吸附试验(ELISA)检测2005年1月至7月哈尔滨医科大学附属第一医院呼吸内科收治的58例COPD患者和同期来医院进行健康体检的30名正常人血清中MMP-9,TIMP-1、ICAM-1和VCAM-1的质量浓度,将MMP-9、TIMP-1和MMP-9/TIMP-1比值与ICAM-1、VCAM-1及第一秒用力呼气容积(FEV1)占预计值百分比(FEV1%)、1秒率(FEV1/FVC%)进行相关性分析。结果(1)COPD患者的MMP-9、TIMP-1、ICAM-1、VCAM-1血清质量浓度[(128.89±115.84),(228.28±107.13),(203.98±70.37),(352.98±117.73)μg/L]明显高于对照组[(30.65±18.43),(133.69±41.41),(148.35±23.77),(233.57±36.65)μg/L],差异均具有显著性意义(P均<0.01)。(2)COPD组血清MMP-9与ICAM-1、VCAM-1质量浓度呈正相关(P均<0.05);血清TIMP-1与ICAM-1、VCAM-1质量浓度呈正相关(P均<0.01);血清MMP-9、TIMP-1、ICAM-1、VCAM-1质量浓度与FEV1%及FEV1/FVC%均呈明显负相关(P均<0.01);MMP-9/TIMP-1比值与FEV1%及FEV1/FVC%均具有明显负相关(P均<0.05)。结论(1)COPD患者血中ICAM-1、VCAM-1增加与MMP-9、TIMP-1增加具有相关性,是COPD发病中基质金属蛋白酶降解细胞外基质的重要调节因素。(2)COPD患者血清MMP-9、TIMP-1明显增加,MMP-9/TIMP-1比值增加,与气流阻塞成负相关,MMP-9、TIMP-1是引起气流阻塞很重要的因素。     

炎性介质在OSAHS与冠心病关系中的作用

采用酶联免疫吸附测定方法检测阻塞型睡眠呼吸暂停低通气综合征（OSAHS）合并冠心病（CHD）、单纯OSAHS患者及健康志愿者血清中细胞间黏附分子1（ICAM-1）、血管细胞黏附分子1（VCAM-1）的水平，采用散射比浊法测定C反应蛋白（CRP）。发现OSAHS＋CHD组和OSAHS组血清ICAM-1、CRP均高于正常对照组；OS-AHS组VCAM-1高于正常对照组；OSAHS＋CHD组CRP高于OSAHS组。OSAHS患者ICAM-1与睡眠呼吸暂停低通气指数呈显著正相关，ICAM-1、VCAM-1均与体质量指数呈正相关。认为血清ICAM-1和CRP水平增高是OS-AHS患者发生CHD的重要危险因子之一。     

黏附分子在沙利度胺所致大鼠肝纤维化中的作用机制

目的:观察沙利度胺对大鼠实验性肝纤维化的治疗效果并探讨其作用机制.方法:四氯化碳腹腔注射制备大鼠肝纤维化模型后,应用沙利度胺(100 mg/kg)ig分别治疗2、4、6 wk作为动态观察时相点.HE染色观察肝组织病理变化,放射免疫法检测血清透明质酸(HA)、层粘连蛋白(LN)、Ⅲ型前胶原(PC Ⅲ)和Ⅳ型胶原(CⅣ)的表达,免疫组织化学法检测细胞间黏附分子-1(ICAM-1)、血管细胞黏附分子-1(VCAM-1)和E-选择素(E-selectin)蛋白质的表达,逆转录聚合酶链反应法检测ICAM-1、VCAM-1和E-selectin mRNA的表达.结果:与肝纤维化组相比,沙利度胺治疗4wk、6 wk能显著降低大鼠肝组织纤维化积分,显著降低血清HA(176.6±7.5 μg/L,173.8±6.7 μg/L vs 486.9±12.4 μg/L)、LN(38.4±5.8 μg/L,34.7±7.3 μg/L vs 84.5±5.2 μg/L)、PC Ⅲ(44.3±5.5 μg/L,40.2±6.1 μg/L vs 65.0±5.6μg/L)、CⅣ(31.8±6.7 μg/L,30.4±5.7 μg/L vs 55.6±6.5 μg/L)的含量(P＜0.05),沙利度胺治疗2 wk 4 wk,6 wk组均可显著降低ICAM-1、VCAM-1和E-selectin蛋白和mRNA的表达(P＜0.05).结论:沙利度胺可通过下调ICAM-1、VCAM-1和E-selectin表达水平而发挥抗肝纤维化作用.     

不稳定型心绞痛患者血清内脏脂肪素水平的变化及与血管内皮细胞黏附分子的相关性

目的观测不稳定型心绞痛(UA)患者血清内脏脂肪素(visfatin)水平的变化,并探讨血清Visfatin与可溶性血管细胞黏附分子1(s VCAM-1)、可溶性细胞间黏附分子1(s ICAM-1)之间的相关性。方法采用定量夹心酶联免疫检测技术对80例UA患者(UA组)、68例稳定型心绞痛(SA)患者(SA组)及60例健康对照者(对照组)血清Visfatin、s VCAM-1、s ICAM-1水平的变化进行检测,同时常规检测其他临床生物化学指标。在UA组,采用Pearson相关检验对血清Visfatin与s VCAM-1、s ICAM-1、高敏C反应蛋白(hs-CRP)及其他生物化学指标进行相关性分析。结果 UA组血清Visfatin、s VCAM-1、s ICAM-1水平显著高于SA组及对照组(P0.05、P0.01)。UA组血清Visfatin水平与s VCAM-1(r=0.332,P0.01)、s ICAM-1(r=0.479,P0.01)、hs-CRP(r=0.521,P0.01)水平呈显著正相关,而与腰围、体质指数、血压及其他生物化学指标无明显相关性。SA组、对照组血清Visfatin、s VCAM-1、s ICAM-1水平没有显著性差异(P0.05)。结论 UA患者血清Visfatin水平显著升高,并与s VCAM-1、s ICAM-1、hs-CRP呈正相关,提示血清Visfatin与血管内皮损伤及斑块的不稳定性密切相关,可能为血管内皮损伤的标志物。     

回医扎里奴思方对痰热腑实证脑缺血再灌注大鼠脑内细胞间黏附分子1和血管间黏附分子1表达的影响

目的探讨扎里奴思方对痰热腑实证脑缺血再灌注大鼠脑内细胞间黏附分子(ICAM)-1和血管间黏附分子(VCAM)-1表达的影响。方法将60只雄性大鼠随机分为假手术组、模型组、尼莫地平组、扎里奴思方组,每组15只;除假手术组外,其余各组均给予高脂喂养4 w后,予10%的自体粪便1 ml/100 g灌胃,1次/d,连续3 d,造成痰热腑实证模型,再采用线栓法制备大脑中动脉阻塞(MCAO)模型;大鼠给药剂量尼莫地平组10.8 mg/kg、扎里奴思方组1.54 g/ml,制备MCAO模型前3 d灌胃给药。大鼠分别于缺血再灌注后1、3、7 d取脑,取材前进行脑组织含水量测定,采用免疫组化法检测缺血侧海马区ICAM-1、VCAM-1的表达,RT-PCR检测ICAM-1 mRNA和VCAM-1 mRNA的表达。结果与假手术组比较,模型组脑组织含水量增高(P<0.01);ICAM-1、VCAM-1阳性细胞,ICAM-1 mRNA、VCAM-1 mRNA表达明显增高(P<0.01)。与模型组比较,尼莫地平组和扎里奴思方组脑组织含水量降低;ICAM-1、VCAM-1阳性细胞数减少,ICAM-1 mRNA、VCAM-1 mRNA表达降低(P<0.01)。与尼莫地平组比较,扎里奴思方7 d组脑组织含水量降低,ICAM-1、VCAM-1阳性细胞数减少,ICAM-1 mRNA、VCAM-1 mRNA表达降低(P<0.05)。结论扎里奴思方对痰热腑实证脑缺血再灌注大鼠脑神经元起保护作用,其机制可能与抑制大鼠脑内ICAM-1和VCAM-1的表达有关。     

胃肿瘤患者循环可溶性细胞间粘附分子-1和血管细胞粘附分子-1

AIM To elucidate the biological and clinical significance of sICAM-1 and sVCAM-1 in patients with gastric cancer.METHODS The serum levels of soluble ICAM-1 and VCAM-1 were measured with sandwith enzyme immunoassay.RESULTS In gastric cancer patients, soluble ICAM-1 and VCAM-1 concentrations were significantly elevated in comparision with those of healthy subjects (289.23μg/L±32.69μg/L vs 190.44μ/L±35.92μg/L,1430.88μg/L±421.71μg/L vs 727.24μg/L±157.68μg/L, respectively, P＜0.01). The increment in serum sICAM-1 and sVCAM-1 concentrations correlated well with the staging of gastric cancer. The serum levels of sICAM-1 and sVCAM-1 in patients of Ⅲ-Ⅳ stages were higher than those of Ⅰ-Ⅱ stages (346.60μg/L±92.10μg/L vs 257.54μg/L±32.77μg/L, 1800.60μg/L±510.76μg/L vs 1262.81μg/L±236.73μg/L). The levels of sICAM-1 and sVCAM-1 were correlated significantly (r=0.49,P＜0.01). The sICAM-1 and sVCAM-1 levels correlated positively with alkaline phophatase (r=0.63,0.71,P＜0.001) and white cell count (r=0.52,0.43, P＜0.01); but correlated negatively with serum albumin (r=-0.41, -0.49, P＜0.01).CONCLUSION The measurement of circulating ICAM-1 and VCAM-1 may bring additional prognostic information for patients with gastric cancer in varying stages.INTRODUCTIONTumor growth and metastasis involves a variety of cell-cell and cell-extracellular matrix interactions mediated by cell adhesion molecules. Currently, a number of cell adhesion molecules, such as intercellular adhesion molecules-1 (ICAM-1), vascular cell adhesion molecules-1 (VCAM-1), etc. have been found.ICAM-1 and VCAM-1 are members of the immunoglobulin supergene family which are cytokine-induced glycoproteins (IL-1, TNFα and IFNγ). Both of them have five or seven extracellular immunoglobulin-like domains, a single transmembranous domain and a short cytoplasmic tail[1,2]. The natural ligand of ICAM-1 or VCAM-1 is LFA-1 (CD11a) and Mac-1 (CD11b) or VLA-4, respectively[3]. ICAM-1 is a widely distributed protein on a variety of tissues, and can be detected in many cells such as macrophage, T- and B-cells, or fibroblasts, endothelial and epithelial cells. VCAM-1 is also a widely distributed protein and is constitutively expressed on tissue macrophage, dentritic cells in lymphoid tissue and skin, as well as on bone marrow fibroblasts and epithelial cells. Expression of VCAM-1 is inducible on vascular endothelial cells under pathological conditions[4].Recently, soluble forms of several adhesion molecules including ICAM-1 and VCAM-1 were found in serum of normal donors[5]. Abnormally high levels of them have been described in some solid malignant tumors, leukemia, autoimmune disease, infectious disease, etc.The present study was carried out to measure the circulating levels of sICAM-1 and sVCAM-1 in gastric cancer before treatment was given and to study their correlation with clinical, histological and routine laboratory parameters.     

细胞黏附分子-1在急性髓性白血病细胞与内皮细胞黏附中的作用

目的　检测急性髓性白血病 (AML)细胞与内皮细胞的黏附及细胞黏附分子 1(ICAM 1)及其配体淋巴细胞功能相关抗原 1(LFA 1)在黏附中的作用。方法　观察AML细胞与静止内皮细胞和肿瘤坏死因子α(TNFα)激活的内皮细胞的黏附 ;AML细胞与内皮细胞混合培养 2 4h的黏附 ;正常中性粒细胞与AML细胞培养上清作用 2 4h后的内皮细胞的黏附 ;流式和ELISA方法检测AML细胞培养上清作用后内皮细胞ICAM 1及可溶性ICAM 1的表达 ;并用ICAM 1和LFA 1的抗体进行阻滞黏附试验。结果　AML细胞与静止的内皮细胞黏附较少 (2 4 33± 2 87) % ,AML细胞与TNFα激活的内皮细胞的黏附 ,与内皮细胞混合培养 2 4h后的黏附以及正常中性粒细胞与AML细胞培养上清作用后内皮细胞的黏附明显增加 ,分别为 (81 87± 4 0 8) % ,(82 0 6± 7 0 5 ) % ,(83 99± 3 86 ) % (n =2 1,P <0 0 0 1) ;静止的内皮细胞ICAM 1及可溶性ICAM 1的表达分别为 (5 5 81± 4 11) %和 (0 839± 0 2 36 )μg/L ;AML细胞培养上清作用后内皮细胞ICAM 1及可溶性ICAM 1的表达明显增加 ,分别为 (6 5 36±5 97) %和 (1 4 2 4± 0 4 6 9) μg/L(n =2 1,P <0 0 5 ) ;用ICAM 1及LFA 1的抗体进行黏附阻滞后 ,AML细胞与TNFα激活的内皮细胞的黏附下降为 (2 0 12±     

2型糖尿病患者糖耐量正常一级亲属血管内皮功能及炎症因子的研究

目的研究2型糖尿病患者一级亲属糖耐量正常者(FDR)的血管内皮功能、炎症因子水平及其影响因素。方法测定31例正常人、57例FDR的血管内皮功能、血浆纤溶酶原激活物抑制物1(PAI1)及血清可溶性血管细胞黏附分子1(VCAM1)水平,同时测定胰岛素水平,计算胰岛素敏感性(IAI)。结果与正常对照组比较,FDR内皮依赖性血管舒张功能减低[(1245±337)%比(503±034)%],IAI降低[(-379±057)比(-411±046)],血浆PAI1水平升高[(3046±1228)μg/L比(3925±654)μg/L],血清VCAM1水平升高[(63731±10732)μg/L比(74239±12431)μg/L],差异均有统计学意义(P值均<005)。结论糖耐量正常的2型糖尿病患者一级亲属胰岛素敏感指数下降、血管内皮功能受损、纤溶活性降低,且血管内皮功能失调与胰岛素抵抗密切相关。     

通心络超微粉对高脂饮食兔胸主动脉NF-κB、胞间黏附分子1及血管细胞黏附分子1表达的影响

目的探讨通心络超微粉对高脂饮食兔胸主动脉NF-κB、胞间黏附分子1（ICAM-1）及血管细胞黏附分子1（VCAM-1）表达的影响。方法健康雄性新西兰白兔32只,随机分为空白对照组、模型组、阿托伐他汀组、通心络组四组。空白对照组,饲以普通饲料;模型组,饲以高脂饲料;阿托伐他汀组,饲以高脂饲料同时阿托伐他汀（3mg·kg^-1·d^-1）灌胃;通心络组,饲以高脂饲料同时通心络超微粉（0．31g·kg^-1·d^-1）灌胃,连续给药,于6周末免疫组织化学染色法检测主动脉壁中NF-κB核转位情况、ICAM-1及VCAM-1蛋白表达情况,RT—PCR法检测ICAM-1 mRNA及VCAM-1 mRNA表达。结果与空白对照组相比,模型组家兔主动脉壁中NF—KB核转位明显增加。ICAM-1、VCAM-1基因及蛋白表达明显增多（P〈O．01）。与模型组相比,通心络组与阿托伐他汀组家兔主动脉壁中NF-κB核转位明显减少、ICAM-1、VCAM-1基因及蛋白表达明显减少（P〈0．01或P〈0．05）,通心络组显著少于阿托伐他汀组（P〈0．01）。结论通心络超微粉通过抑制NF-κB核转位进而降低ICAM-1、VCAM-1基因及蛋白表达,减轻动脉粥样硬化病理改变。     

可溶性血管细胞黏附分子-1与2型糖尿病及其并发症的相关性研究

目的探讨血清可溶性血管细胞黏附分子-1(sVCAM-1)与2型糖尿病及其并发症的关系.方法采用酶联免疫吸附法测定61例合并高血压和微血管并发症的糖尿病患者及36例正常人血清中sVCAM-1水平.结果2型糖尿病患者的sVCAM-1水平[(973.25±73.38)μg/L]明显高于非糖尿病患者[(230.45±12.47)μg/L],P＜0.001.合并高血压患者sVCAM-1[(1263.99±87.00)μg/L]较微血管病变者[(726.57±95.40)μg/L]增高更明显(P＜0.001).结论sVCAM-1参与了糖尿病血管并发症的发生和发展.     

Analysis of adhesion molecules in patients with idiopathic portal hypertension

BACKGROUND: The aetiology of idiopathic portal hypertension (IPH) is unknown. However, some evidence of immunological abnormalities in IPH patients has been reported. METHODS: As adhesion molecules are important in the interaction between lymphocytes and accessory and target cells, the expression and release of the soluble form of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule (ICAM-1) were examined in this study. RESULTS: In IPH patients, the serum level of soluble VCAM-1 was found to be increased, compared with that of healthy subjects, fatty liver patients and chronic hepatitis patients. The level of soluble ICAM-1 of IPH patients was found to be slightly increased, compared with that of healthy subjects; however, it was not different from the level in patients with other diseases. The expression of VCAM-1 was observed in the sinusoidal lining cells and endothelial cells around the liver vessels of several IPH patients. In contrast, ICAM-1 was weakly expressed in sinusoidal lining cells and hepatocytes in the liver tissue of only one of four IPH patients. CONCLUSIONS: This differential pattern of VCAM-1 and ICAM-1 was found in IPH patients and it was suggested that VCAM-1 might be an important molecule in the occurrence of IPH.     

Soluble cell adhesion molecules in hypertensive concentric left ventricular hypertrophy

OBJECTIVE : Concentric left ventricular (LV) hypertrophy is an important cardiovascular risk factor. We investigated whether concentric LV hypertrophy is associated with activation of the vascular endothelium, as assessed by measurements of soluble cell adhesion molecules. DESIGN : E-selectin, intercellular adhesion molecule-1 (ICAM-1), and vascular adhesion molecule-1 (VCAM-1) were measured in serum from hypertensive patients with LV hypertrophy (64 with concentric and 47 with eccentric hypertrophy) and from two matched control groups consisting of 38 hypertensive patients without LV hypertrophy and 38 normotensive subjects. Carotid artery intima-media thickness (IMT) was examined by ultrasonography and LV mass by echocardiography. Neurohormone activities of the renin-angiotensin-aldosterone system were also measured. RESULTS : E-selectin levels were higher in hypertensive than in normotensive subjects (56 +/- 19 versus 49 +/- 11 ng/ml, P = 0.031). Patients with concentric LV hypertrophy had higher levels of E-selectin (61 +/- 21 versus 49 +/- 15 ng/ml, P < 0.001), ICAM-1 (273 +/- 49 versus 254 +/- 49 ng/ml, P = 0.043), VCAM-1 (591 +/- 131 versus 544 +/- 78 ng/ml, P = 0.038) and greater carotid artery IMT (0.99 +/- 0.26 versus 0.83 +/- 0.15 mm, P = 0.018) than eccentric LV hypertrophy patients. E-selectin and VCAM-1 correlated positively to LV relative wall thickness (P = 0.040 and 0.037, respectively), with a similar trend for ICAM-1 (P = 0.083). E-selectin correlated with serum aldosterone (P < 0.001), and E-selectin and ICAM-1 with plasma angiotensin converting enzyme activity (P = 0.003 and 0.036, respectively). CONCLUSION : Increased levels of soluble cell adhesion molecules and an increased carotid artery IMT characterize concentric LV hypertrophy. This indicates perturbations at the vascular level, involving activation of the vascular endothelium in hypertensive patients with concentric LV hypertrophy.     

Circulating adhesion molecules in patients with virus-related chronic diseases of the liver

AIM:In the inflammatory state, intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1) play a key role in promoting migration of immunological cells from the circulation to target site. Aim of our study was to investigate soluble forms of these molecules in patients with virus-related chronic liver diseases, to assess their behavior in different pathologies and correlation with severity of liver damage. METHODS:Circulating ICAM-1 and VCAM-1 were assayed by EIA commercial kits (R&D System Co., Abington, UK) in 23 patients with chronic active hepatitis (CH), 50 subjects affected by liver cirrhosis (LC) and 15 healthy controls comparable for sex and age. In patients, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were also detected by autoanalyzer. RESULTS:LC patients had significantly higher ICAM-1 values than CH patients (38.56±7.4 ng/mL Vs20.89±6.42 ng/mL; P<0.001) and these ones had significantly higher values than controls (12.92±1.08 ng/mL; P<0.001). In CH group, ICAM-1 levels were significantly related to inflammatory activity (P=0.041) and ALT values (r=0.77; P<0.05). VCAM-1 values were significantly increased only in LC patients (P<0.001) and related to severity of liver impairment. CONCLUSION:These findings suggest that the determination of serum ICAM-1 can be considered as an additional useful marker of hepatocellular necrosis and inflammatory activity in chronic hepatitis, while serum VCAM-1 is an indicator of liver fibrogenesis and severity of disease in cirrhosis.     

Mechanisms of high-density lipoprotein cholesterol effects on the endothelial function in hyperlipemia

High-density lipoprotein-cholesterol (HDL-c) has a favorable influence on the endothelial function, but the mechanisms of this protective action are not fully understood. We studied lipid parameters, soluble adhesion molecules (vascular cell adhesion molecule-1 [VCAM-1], intercellular adhesion molecule [ICAM-1], E-selectin) oxidized low-density lipoproteins (LDL), and brachial-artery flow-mediated vasodilation (FMV) in 184 hyperlipemic patients (90 men, age 54 +/- 10 years, waist/hip circumference ratio 0.89 +/- 0.07, LDL-cholesterol [LDL-c] 4.9 +/- 1.3 mmol/L, triglycerides 1.8 +/- 0.9 mmol/L, HDL-c 1.3 +/- 0.5 mmol/L) after excluding those with current smoking, diabetes, hypertension, and vascular diseases. Patients were divided into 2 groups on the basis of HDL-c levels: < 1.03 mmol/L (n = 53) v >or= 1.03 mmol/L (n = 131). Patients with low HDL-c showed significantly lower LDL-c (P <.05), higher triglycerides (P <.001), higher body mass index (P <.02), lower FMV (3.7% +/- 2.0% v 4.9% +/- 3.4%, P <.002), higher VCAM-1 (1,195 +/- 395 ng/mL v 984 +/- 303 ng/mL, P <.01), and higher ICAM-1 (406 +/- 78 ng/mL v 364 +/- 68 ng/mL, P <.01). E-selectin and oxidized LDL showed no significant differences. In a multivariate age, oxidized LDL and brachial artery diameter predicted a lower FMV, while HDL-c was an independent predictor of a greater FMV (P =.003). Increasing levels of VCAM-1 and ICAM-1 were predicted by lower HDL-c, while higher oxidized LDL predicted higher VCAM-1 (P <.05). Our data suggest that in hyperlipemic subjects free of cardiovascular disease low HDL-c negatively modulates endothelial function through a lack of oxidation inhibition and a concomitant overexpression of adhesion molecules.