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1.
目的 观察冠心病患者血清晚期糖基化终产物(AGE)Nε-羧甲基赖氨酸(CML)的水平.方法 采用抗戚蓝蛋白晚期糖基化终产物(KLH-AGE)抗体竞争ELISA法,对33例冠心病患者、14例单纯高血压患者及38名正常人血清中CML进行定量观察.结果 33例冠心病患者血清中均测得CML,正常对照组中仅3名血清CML含量>0.1 mg/L,两组比较差异有极显著性意义(P<0.001).合并高血压的冠心病患者血清CML水平为(0.92±0.61)mg/L,较单纯高血压[(0.23±0.16)mg/L]或单纯冠心病[(0.44±0.47)mg/L]患者明显增高(P<0.01,P<0.05).不合并糖尿病的冠心病患者和合并糖尿病的冠心病患者血清CML水平无显著差异.结论 冠心病患者血清CML水平明显增高,提示机体内晚期糖基化终产物的产生在冠状动脉粥样硬化的形成机制中可能起一定的作用.血清CML含量可作为冠心病患者晚期糖基化反应水平的生物学指标.  相似文献   

2.
目的探讨可溶性血管细胞黏附分子1(sVCAM-1)在肺结核发病机制中的作用和临床意义,及其与肿瘤坏死因子α(TNF-α)和γ干扰素(IFN-γ)的关系。方法采用酶联免疫吸附测定(ELISA)法检测未经治疗的35例肺结核患者(肺结核组)、20名健康人(对照组)血清 sVCAM-1、IFN-γ水平,放射免疫分析(RIA)法测定血清 TNF-γ水平。肺结核组中,血型播散性肺结核(Ⅱ型)15例,继发性肺结核(Ⅲ型)20例,后者于治疗2个月后再次采血。结果肺结核组血清 sVCAM-1、TNF-γ和 IFN-γ的水平分别为(822±206)、(1.5±1.1)和(23±13)μg/L,高于对照组(428±73)、(0.2±0.1)和(16±10)μg/L,差异有统计学意义(P 值分别<0.01、<0.01、<0.05);血型播散性肺结核(Ⅱ型)患者的血清 sVCAM-1和 TNF-α的水平分别为(897±144)、(2.0±1.4)μg/L,高于继发性肺结核(Ⅲ型)患者的(765±230)和(1.2±0.6)μg/L,差异有统计学意义(P 值均<0.05);IFN-γ在Ⅱ型与Ⅲ型肺结核患者之间差异无统计学意义(P=0.222)。抗结核治疗后,血清 sVCAM-1和TNF-α水平分别为(532±103)、(0.8±0.8)μg/L,与治疗前相比差异有统计学意义(P 值均<0.01);治疗2个月后 sVCAM-1和 TNF-α水平仍高于对照组(P<0.01);IFN-γ治疗后水平高于治疗前(P<0.05)。肺结核治疗前血清 sVCAM-1与 TNF-α、IFN-γ均呈正相关(r 值分别为0.669、0.560,P 值均<0.01)。对照组和肺结核组治疗后血清 sVCAM-1与 TNF-α、IFN-γ之间均无相关性。结论sVCAM-1可以作为判断病情严重程度和评价疗效的一项临床指标。  相似文献   

3.
目的 :探讨血脂异常对血清细胞间黏附分子 1(ICAM 1)、血管细胞黏附分子 1(VCAM 1)和E 选择素水平的影响。方法 :入选 12 0例研究对象 ,其中高胆固醇血症 (Ⅰ组 ) 31例 ;高三酰甘油血症 (Ⅱ组 ) 30例 ;混合性高脂血症 (Ⅲ组 ) 2 9例 ;血脂正常 (Ⅳ组 ) 30例。用酶联免疫吸附法检测血清ICAM 1、VCAM 1和E 选择素水平 ,比较上述 3个指标在各组间的差异。结果 :总胆固醇水平 ,Ⅰ组 [(6 .5 5± 0 .6 7)mmol/L]和Ⅲ组 [(6 .2 7±0 .6 7)mmol/L]显著高于Ⅳ组 [(4.38± 0 .4 9)mmol/L],P <0 .0 1;三酰甘油水平 ,Ⅱ组 [(3.39± 0 .6 0 )mmol/L]和Ⅲ组 [(3.4 4± 0 .6 2 )mmol/L]显著高于Ⅳ组 [(1.39± 0 .4 0 )mmol/L],P <0 .0 1。同时 ,血清ICAM 1水平在Ⅰ组 [(76 4± 71) μg/L]、Ⅱ组 [(74 9± 71) μg/L]和Ⅲ组 [(82 3± 80 ) μg/L]明显高于Ⅳ组 [(6 0 4± 6 7) μg/L],P <0 .0 1;血清VCAM 1水平在Ⅰ组 [(1837± 16 4 ) μg/L]、Ⅱ组 [(1836± 16 0 ) μg/L]和Ⅲ组 [(196 3± 181) μg/L]明显高于Ⅳ组 [(130 7± 14 9) μg/L],P <0 .0 1;血清E 选择素水平在Ⅰ组 [(6 6± 12 ) μg/L]、Ⅱ组 [(70± 14 ) μg/L]和Ⅲ组 [(81± 17) μg/L]明显高于Ⅳ组 [(39± 11) μg/L],P <0 .0 1。结论 :血脂异常可使血清I  相似文献   

4.
目的 探讨2型糖尿病合并大血管病变患者的血清瘦素水平及其临床意义.方法 采用酶联免疫吸附法测定健康对照组、2型糖尿病合并大血管病变组和2型糖尿病未合并大血管病变组患者的血清瘦素水平.结果 2型糖尿病合并大血管病变组患者的瘦素水平显著高于未合并大血管病变组[(10.12 ±3.44)μg/L比(7.99 ±3.18) μg/L,P<0.05]和对照组[(10.12±3.44)μg/L比(6.04±1.86) μg/L,P<0.01].结论 2型糖尿病合并大血管病变的患者血清瘦素水平明显升高,瘦素与糖尿病大血管病变密切相关.  相似文献   

5.
目的研究老年心力衰竭患者血清细胞因子水平与心功能的关系以及雷米普利对血清细胞因子的影响.方法将76例老年心力衰竭患者随机分为雷米普利治疗组(36例)和常规治疗组(40例),另设年龄、性别与之匹配的健康老年人作为对照组(30例).应用双抗夹心ELISA法检测各组受试者血清肿瘤坏死因子α(TNF-α)、可溶性肿瘤坏死因子受体(STNFRI)、白细胞介素6(IL-6)、白细胞介素10(IL-10)和转化生长因子β1(TGF-β1)水平.常规治疗组和雷米普利组在治疗2周后复查上述指标.结果(1)血清TNF-α、STNFRI、IL-6、IL-10和TGF-βI水平与老年心力衰竭患者的基础心脏病无关(P<0.05);上述血清细胞因子水平随心功能的恶化而升高(P<0.05或P<0.01).(2)与治疗前比较,雷米普利治疗组治疗前后血清TNF-α[(20.9±8.2)μg/L比(13.2±8.4)μg/L]、sTNFRI[(2.7±0.9)μg/L比(1.9±0.4)μg/L]、IL-6[(29.2±6.8)ng/L比(20.5±6.0)ng/L]、IL-10[(22.1±6.4)ng/L比(13.8±5.7)ng/L]及TGF-β1[(2144.1±597.9)ng/L比(1348.8±342.4)ng/L]水平均下降(分别为P<0.05或P<0.01),雷米普利治疗组比常规治疗组下降明显(P<0.01).结论老年心力衰竭患者血清细胞因子与心功能密切相关,能够反映心力衰竭的程度;雷米普利能明显改善老年心力衰竭患者细胞因子的异常.  相似文献   

6.
目的探讨高血压病患者血清可溶性E-选择素(sE-Selectin)浓度与肥胖、性别、血糖、胰岛素等的关系.方法酶联免疫吸附法测定179例原发性高血压患者(正常体重组43例,超重组104例,肥胖组32例;男67例,女112例)和29例正常体重和血压者(对照组,男11例,女18例)的空腹血清sE-se-lectin浓度,口服葡萄糖耐量试验和胰岛素释放试验,测定血浆葡萄糖浓度和血清胰岛素浓度,计算葡萄糖曲线下面积(AUCG)和胰岛素曲线下面积(AUCIN),测定收缩压、舒张压和体重指数(BMI).分析血清sE-slectin浓度与其它各项参数的相关性.结果血清sE-slectin浓度对照组(35.2±15.0)μg/L和正常组(37.8±12.9)μg/L无显著差异(P>0.05),肥胖组(56.4±21.2)μg/L高于超重组(43.5±16.6)μg/L(P<0.001)、正常组(P<0.001)和对照组(P<0.001),高血压患者男性组(50.0±17.8)μg/L高于女性组(41.2±16.9)μg/L(P<0.01).高血压患者血清sE-slectin浓度男性组与BMI相关,女性组与BMI、空腹胰岛素、AUCIN相关.结论肥胖和男性高血压病患者有较高的血清sE-Slectin浓度,肥胖程度与血清sE-slectin浓度直接正相关,提示肥胖和男性高血压病患者可能有较高的血管内皮细胞活化程度.  相似文献   

7.
目的探讨糖尿病伴高血压患者血浆心肌营养素-1(CT-1)的变化及作用.方法应用生物素-链霉亲和素酶联免疫吸附测定法(BSA-ELISA)测定35名正常健康人、25例2型糖尿病患者及57例2型糖尿病伴高血压患者血浆CT-1水平.结果3组间血浆CT-1水平差异有显著性,糖尿病伴高血压组血浆CT-1水平(269.3±65.3)pg/mL显著高于2型糖尿病组(99.5±27.2)pg/mL及正常对照组(31.5±9.7)pg/mL(P<0.001);2型糖尿病组高于正常组(P<0.05).Pearson相关分析结果显示血浆CT-1水平与收缩压(r=0.660,P<0.001)、舒张压(r=0.428,P<0.001)、甘油三酯(r=0.403,P<0.001)、载脂蛋白B(r=0.335,P<0.001)、载脂蛋白A(r=0.189,P<0.001)、总胆固醇(r=0.183,P<0.05)、低密度脂蛋白(r=0.171,P<0.05)相关.多元逐步回归分析发现影响血浆CT-1水平的最显著因素为收缩压、舒张压及载脂蛋白B.结论糖尿病患者血浆CT-1水平升高表明糖尿病发生发展过程中已开始有心血管病变的进行,糖尿病伴高血压患者更为明显.  相似文献   

8.
目的 探讨急性冠脉综合征(ACS)病人可溶性细胞间黏附分子-1(sICAM-1)、血管细胞黏附分子-1(sVCAM-1)和C反应蛋白(CRP)水平及通心络胶囊的干预作用.方法 选取ACS病人63例,将其分为常规治疗组(A组)和通心络治疗组(B组).B组在常规治疗基础上加服通心络胶囊.另选健康成人30例为正常对照组(C组).采用酶联免疫吸附法测定各组sICAM-1和sVCAM-1水平,采用免疫浊度法测定CRP浓度,并对其结果进行比较.结果 ACS病人循环血中sICAM-1、sVCAM-1和CRP水平明显高于正常对照组(P<0.01),A组治疗后sICAM-1、sVCAM-1和CRP水平分别为(196.72±67.53)μg/L、(948.42±436.25)μg/L、(7.15±2.02)mg/L均较治疗前明显下降(P<0.05和P<0.01).B组治疗后3项指标分别为(162.08±48.16)μg/L、(645.31±306.18)μg/L、(5.68±1.76)mg/L均较治疗前明显下降(P<0.01),且A组与B组各项指标比较,B组降低更明显(P<0.05和P<0.01).结论 ACS病人血清中sICAM-1、sVCAM-1和CRP水平明显升高,通心络胶囊能明显降低ACS病人血中sICAM-1、sVCAM-1和CRP水平.  相似文献   

9.
叶酸缺乏对大鼠同型半胱氨酸水平及动脉损伤的影响   总被引:5,自引:1,他引:4  
目的观察叶酸缺乏饮食对大鼠血浆同型半胱氨酸(Hcy)水平及动脉组织的影响.方法雄性Wistar大鼠20只均分成2组,分别给予叶酸缺乏(叶酸缺乏组)和叶酸正常(对照组)饲料,饲养3个月后检测血清叶酸和血浆Hcy浓度及红细胞超氧化歧化酶(SOD)和谷胱甘肽过氧化物酶(GPX)活力,实验后光镜检查主动脉组织学变化.结果叶酸缺乏组实验后血清叶酸浓度[(6.08±1.84)μg/L]明显低于实验前[(13.32±2.02)μg/L]和对照组[(12.17±1.67)μg/L],而血浆Hcy浓度[(28.66±6.07)μmol/L]明显高于实验前[(9.75±1.86)μmol/L]和对照组[(9.49±1.77)μmol/L,P<0.01];红细胞SOD[(37389.5±5158.4)NU/g*Hb]高于对照组[(30355.7±6349.2)NU/g*Hb],GPX活力[(10.94±3.05)U/L]低于对照组[(17.93±3.05)U/L,P<0.05];主动脉组织出现内皮细胞肿胀、变性、脱落,裸露的内膜附有血栓和胶原纤维,内皮下组织疏松并出现平滑肌细胞,内弹力膜断裂,中膜明显增厚.结论叶酸缺乏饮食可引发高Hcy血症和动脉损伤,高Hcy血症诱导体内高氧化应激可能是动脉损伤机制之一.  相似文献   

10.
目的 探讨血清骨桥蛋白水平与舒张性心力衰竭的关系.方法 入选患者67例,其中对照组22例,单纯高血压组22例,高血压合并舒张性心力衰竭组23例.入院时测量血压,同时应用心脏彩超检测患者E峰、A峰、E/A比值、左室射血分数(LVEF)、室间隔侧二尖瓣瓣环E '(舒张早期二尖瓣环运动速度).采用ELISA法检测血清OPN水平.比较三组间血清OPN浓度的变化.结果 高血压合并舒张性心力衰竭组血清OPN浓度[(143.82±43.67) μg/L]高于对照组[(117.10 ±34.64)μg/L]及单纯高血压组[(114.53±26.55) μg,/L],差异具有统计学意义(P<0.05).对照组与单纯高血压组血清OPN浓度差异无统计学意义(P>0.05).高血压合并舒张性心力衰竭患者血清OPN浓度与E/E’值呈正相关.血清OPN浓度均值心功能Ⅱ级组[(107.76±36.51) μg/L]<心功能Ⅲ级组[(143.67±16.76)μg/L]<心功能Ⅳ级组[(180.02±37.90) μg/L],差异具有统计学意义(P<0.05).结论 高血压合并舒张性心力衰竭患者的血清OPN浓度增高,与E/E’值呈正相关,并随心功能分级升高而增加.  相似文献   

11.
目的 探讨可溶性血管细胞黏附分子-1(sVCAM-1)和可溶性血小板内皮细胞黏附分子-1(sPECAM-1)在COPD发病中的作用.方法 病例为2005年12月至2006年3月在遵义医学院附属医院呼吸科住院患者.采用酶联免疫吸附测定法,检测20例健康成人(对照组)和35例COPD急性加重期(AECOPD)患者治疗前后血浆D-二聚体、sVCAM-1和sPECAM-1水平.统计学处理采用t检验和Pearson直线相关分析.结果 AECOPD治疗前组D-二聚体[(4.49±1.47)mg/L]明显高于治疗后组[(1.98±0.92)mg/L]和对照组[(0.44±0.14)mg/L],治疗后组也明显高于对照组;治疗前组sVCAM-1[1(11±5)nmol/L]明显高于治疗后组[(8±4)nmol/L]和对照组[(7±4)nmol/L];治疗后组sPECAM-1[(61±13)pmol/L]明显高于治疗前组[(36±8)pmol/L]和对照组[(43±10)pmol/L],对照组也明显高于治疗前组;治疗前sVCAM-1与D-二聚体呈正相关(r=0.759,P<0.01),治疗前sPECAM-1与D-二聚体、sVCAM-1均无直线相关性(r值分别为0.045和0.078,P均>0.05);治疗后sPECAM-1与D-二聚体呈负相关(r=-0.548,P<0.01),治疗后sVCAM-1与D-二聚体、sPECAM-1均无直线相关性(r值分别为-0.032、0.143,P均>0.05);对照组D-二聚体、sVCAM-1及sPECAM-1三者之间均无直线相关性(r值分别为0.137、-0.121和0.035,P均>0.05).结论 D-二聚体、sVCAM-1在AECOPD显著增高,表明AECOPD存在血栓前状态,提示D-二聚体和sVCAM-1可作为判断AECOPD并发血栓前状态及其严重程度的指标;sPECAM-1在治疗后显著增高,可能作为一种保护性因子起对抗血栓前状态的作用.  相似文献   

12.
AIMS: To determine in Type 1 diabetes patients if levels of pigment epithelium-derived factor (PEDF), an anti-angiogenic, anti-inflammatory and antioxidant factor, are increased in individuals with complications and positively related to vascular and renal dysfunction, body mass index, glycated haemoglobin, lipids, inflammation and oxidative stress. METHODS: Serum PEDF levels were measured by ELISA in a cross-sectional study of 123 Type 1 diabetic patients (71 without and 52 with microvascular complications) and 31 non-diabetic control subjects. PEDF associations with complication status, pulse-wave analysis and biochemical results were explored. RESULTS: PEDF levels [geometric mean (95% CI)] were increased in patients with complications 8.2 (7.0-9.6) microg/ml, vs. complication-free patients [5.3 (4.7-6.0) microg/ml, P < 0.001] and control subjects [5.3 (4.6-6.1) microg/ml, P < 0.001; anova between three groups, P < 0.001], but did not differ significantly between control subjects and complication-free patients (P > 0.05). In diabetes, PEDF levels correlated (all P < 0.001) with systolic blood pressure (r = 0.317), pulse pressure (r = 0.337), small artery elasticity (r = -0.269), glycated haemoglobin (r = 0.245), body mass index (r = 0.362), renal dysfunction [including serum creatinine (r = 0.491), cystatin C (r = 0.500)], triglycerides (r = 0.367), and inflammation [including log(e)C-reactive protein (CRP; r = 0.329), and soluble vascular cell adhesion molecule-1 (r = 0.363)]. Age, blood urea nitrogen, systolic blood pressure, pulse pressure and log(e)CRP correlated with PEDF levels in control subjects (all P < 0.04). PEDF levels were not significantly correlated with measures of oxidative stress: isoprostanes, oxidized low-density lipoprotein or paraoxonase-1 activity. On stepwise linear regression analysis (all subjects), independent determinants of PEDF levels were renal function, triglycerides, inflammation, small artery elasticity and age (r(2) = 0.427). CONCLUSIONS: In Type 1 diabetes, serum PEDF levels are associated with microvascular complications, poor vascular health, hyperglycaemia, adiposity and inflammation.  相似文献   

13.
Chen SC  Song GY  Wang SJ  Ye W  Ma BQ 《中华内科杂志》2005,44(3):165-168
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。  相似文献   

14.
目的 探讨细胞黏附分子在阻塞性睡眠呼吸暂停低通气综合征(OSAHS)合并高血压(HT)发病中的作用。方法 应用酶联免疫吸附测定(ELISA)方法检测30例OSAHS血压正常患者(OSAHS组)、30例OSAHS合并高血压患者(OSAHS HT组)及30名健康者(正常对照组)血清中可溶性胞间黏附分子1(ICAM-1)、血管细胞黏附分子1(VCAM-1)和L-选择素的含量。结果 OSAHS HT组及OSAHS组患者血清可溶性ICAM-1[分别为(601±406)μg/,L、(513±244)μg/L]、VCAM-1含量[分别为(578±176)μg/L、(480±144)μg/L]均明显高于正常对照组[分别为(355±119)μg/L、(310±163)μg/L,q值分别为4.78,3.07;9.09,5.76,P<0.01],差异有显著性;而L-选择素与对照组相比,差异无显著性(P>0.05);OSAHS HT组的VCAM-1明显高于OSAHS组(q值为3.32,P<0.05),差异有显著性;ICAM-1水平与睡眠呼吸暂停低通气指数(AHI)及微觉醒指数呈明显的正相关(r=0.465,P<0.01,r=0.226,P<0.05);与最低血氧饱和度呈明显的负相关(r=-0.368,P<0.01)。结论 血清ICAM-1、VCAM-1水平的升高是OSAHS患者高血压发病的重要危险因子之一。  相似文献   

15.
Relatives of subjects with type 2 diabetes carry an increased risk for diabetes and cardiovascular disease. Oxidative modification of low-density lipoprotein (LDL) and proinflammatory processes are believed to have central roles in atherogenesis. We have investigated the susceptibility of LDL to oxidation and circulating cell adhesion molecules in healthy, glucose-tolerant adults (aged 18 to 38 years) with (12 men, 2 women) and without (controls; 12 men, 2 women) a parental history of type 2 diabetes. From fasting blood samples, oxidation of LDL was initiated with copper ions and adhesion molecules were measured using immunoassays. Groups were similar with respect to age, body mass index (BMI), blood pressure, plasma glucose, and serum lipids. Resistance of LDL to oxidation was reduced in offspring of parents with type 2 diabetes (time to Vmax, 80.1 +/- 2.2 v 91.4 +/- 2.6 minutes, P =.003). Plasma hydroperoxides did not differ between groups (1.2 +/- 0.1 v 1.1 +/- 0.1 micromol/L). Soluble intracellular adhesion molecule-1 (sICAM1) was elevated in offspring compared with controls (571 +/- 20 v 447 +/- 20 microg/L, P =.0002). Soluble vascular cell adhesion molecule-1 (sVCAM-1) (1,184 +/- 76 v 1084 +/- 56 microg/L, P =.31) and E-selectin (53 +/- 8 v 53 +/- 7 microg/L, P =.98) did not differ between groups. Reduced resistance of LDL to oxidation and increased circulating sICAM-1 in young healthy adult offspring of parents with type 2 diabetes may be intrinsic to increased risk of atherosclerosis in these subjects.  相似文献   

16.
AIMS: To investigate the effects of glycaemic control on insulin sensitivity and serum concentrations of soluble vascular cell adhesion molecule (sVCAM)-1 and E-selectin (sE-selectin) in patients with Type 2 diabetes mellitus. To examine whether reductions in serum adhesion molecule levels correlate with improvement in insulin resistance. METHODS: A total of 54 patients with Type 2 diabetes were treated for 4 weeks with either diet alone, sulphonylurea or insulin. Fasting glucose, insulin sensitivity, lipids, sVCAM-1, and sE-selectin levels were measured before and after treatment. RESULTS: All treatment modalities successfully corrected hyperglycemia. Reductions in blood glucose levels resulted in improvement in insulin sensitivity (diet KITT 2.40 +/- 0.26-3.09 +/- 0.36, P < 0.01; sulphonylurea 2.24 +/- 0.16-2.94 +/- 0.18, P < 0.01; insulin 1.68 +/- 0.27-2.16 +/- 0.22%/min, P < 0.05), and decrease in sE-selectin levels (diet 88.4 +/- 14.9-66.2 +/- 10.8, P < 0.05; sulphonylurea 85.1 +/- 11.6-59.8 +/- 7.8, P < 0.01; insulin 84.4 +/- 8.7-66.8 +/- 7.4 ng/ml, P < 0.01), but no change in sVCAM-1 levels. There was a significant correlation between the degree of decrease in sE-selectin levels and improvement in insulin sensitivity (r = -0.38, P < 0.01). CONCLUSIONS: Correction of hyperglycaemia, independent of treatment modality, resulted in improvement of insulin resistance and decrease in sE-selectin levels. These changes might, in part, contribute to reduce the risk of diabetic microvascular and macrovascular complications in patients with Type 2 diabetes mellitus.  相似文献   

17.
BACKGROUND: Risk factors for atherosclerosis such as hypertension, type 2 diabetes, obesity and dyslipidemia affect endothelial function and stimulate adhesion molecules expression. The aim of the study was to examine endothelial activation in type 2 diabetes and hypertension as indicated by adhesion molecule levels and further to investigate whether the coexistence of the above conditions has a different effect. METHODS: Serum levels of soluble E-selectin, ICAM-1 and VCAM-1 were measured in 17 hypertensive type 2 diabetic patients (DM-HY), 32 normotensive type 2 diabetic patients (DM), 11 hypertensive nondiabetic patients (HY) and 15 healthy subjects. RESULTS: In diabetic patients (either DM-HY or DM), soluble E-selectin levels were significantly increased compared to healthy subjects (p<0.001). In HY patients, both sE-selectin (66.44+/-71.59 vs. 29.42+/-15.56 ng/ml, p=0.033) and sVCAM-1 (1529+/-433.33 vs. 1027+/-243.56 ng/ml, p=0.03) levels were found significantly higher compared to healthy subjects (p<0.05). The coexistence of diabetes and hypertension (DM-HY) did not have an additive effect on circulating adhesion molecules levels compared with the levels observed in either diabetes or hypertension. Systolic and diastolic blood pressure (BP) were independent factors correlated respectively with sE-selectin and sVCAM-1 levels (R=0.454, p=0.034 and R=0.578, p=0.005) in nondiabetic subjects (hypertensive and normotensive). CONCLUSIONS: Type 2 diabetes mellitus and hypertension induce endothelial activation as indicated by elevated levels of soluble adhesion molecules. This effect is not different when comorbidity is present.  相似文献   

18.
国产比索洛尔对高血压2型糖尿病患者糖代谢的影响   总被引:4,自引:0,他引:4  
目的观察国产比索洛尔对高血压合并2型糖尿病患者糖代谢及血压的影响情况。方法将符合纳入标准的高血压合并2型糖尿病患者随机分组。观察治疗前后患者糖化血红蛋白(HbA1c)、空腹血糖、糖耐量和血压等的变化。结果共有92例患者完成研究,其中比索洛尔组47例,卡托普利组45例。治疗前和经12周治疗后两组HbA1c、空腹血糖、餐后2h血糖、收缩压和舒张压差异均无统计学意义(P=0.05)。结论本研究表明比索洛尔作为高选择性β1受体阻滞剂,对于原发性高血压合并2型糖尿病患者糖代谢无明显不良影响,同时具有良好的降压效果。  相似文献   

19.
血管内皮生长因子和内皮素在低氧性肺血管重建中的作用   总被引:18,自引:0,他引:18  
目的探讨血管内皮生长因子(VEGF)和内皮素(ET)-1在低氧性肺动脉高压(HPH)及其肺血管重建中的作用,并观察钾通道开放剂(pinacidil)对HPH的防治作用及对VEGF和ET-1的影响.方法Wister大鼠46只,随机分为3组,对照组15只,低氧组16只,治疗组15只.缺氧组和治疗组大鼠缺氧[氧浓度为(10.0±0.5)%]4周,每天缺氧8h,其中治疗组大鼠于每天缺氧前腹腔注射pinacidil3mg/kg.缺氧4周后测定各组大鼠血清VEGF和血浆ET-1水平、平均肺动脉压(mPAP)、右心室(RV)/[左心室(LV)+室间隔(S)]比值及肺小动脉病理及其形态计量学.结果(1)缺氧组大鼠血清VEGF[(118.73±55.40)ng/L]和血浆ET-1[(221.2±56.2)ng/L]水平明显高于对照组(P<0.01);缺氧组较对照组mPAP升高,RV/(LV+S)比值增高,肺小动脉血管壁显著增厚,管腔明显狭窄.(2)治疗组大鼠血清VEGF[(78.20±16.45)ng/L]和血浆ET-1[(181.6±30.5)ng/L]水平明显低于缺氧组(P<0.01);治疗组较缺氧组mPAP下降(P<0.01),肺小动脉血管壁增厚、管腔狭窄等明显减轻,但治疗组上述各指标仍未完全恢复到对照组水平.结论VEGF和ET-1在HPH及其肺血管重建中发挥重要作用,钾通道开放剂对HPH及其肺血管重建具有一定的逆转作用.  相似文献   

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