一氧化氮和血管紧张素Ⅱ在原发性高血压中的作用

目的：探讨一氧化氮（NO）和血管紧张素Ⅱ（AngⅡ）与原发性高血压（EH）的关系。方法：分别选择EH合并左室肥厚（LVH）患者（EH＋LVH组）、EH无LVH患者（EH组）及正常人（正常对照组）各30例,检测NO、AngⅡ水平,并进行组间比较分析。结果：（1）EH＋LVH组NO水平明显低于EH组、正常对照组[（37.24±11.27）μmol/L比（51.79±20.04）μmol/L比（80.25±20.58）μmol/L],且EH组NO水平明显低于正常对照组（P均〈0.01）;EH＋LVH组AngⅡ水平明显高于EH组、正常对照组[（198.37±93.54）ng/L比（139.87±56.39）ng/L比（57.34±18.85）ng/L],且EH组AngⅡ水平明显高于正常对照组（P〈0.05～〈0.01）;（2）直线相关分析显示收缩压、舒张压与NO呈负相关（r=-0.448、P=0.000;r=-0.249,P=0.018）,与AngⅡ呈正相关（r=0.491,P=0.000;r=0.265,P=0.012）,NO与AngⅡ呈负相关（r=-0.555,P=0.000）。结论：一氧化氮、血管紧张素Ⅱ参与了原发性高血压发病的病理生理过程。     

白大衣高血压患者的血小板功能

目的:探讨白大衣高血压(WCH)患者的血小板功能.方法:选初诊的原发性高血压(EH)患者、 WCH 患者、正常血压(NT)者各35例,通过诊室血压测量和24 h动态血压监测,同时测定并比较3组血小板最大聚集率(PAGTmax)、血浆血小板α-颗粒膜蛋白(GMP-140)含量、平均血小板容积(MPV) 、血小板数量的变化.结果:和NT对照组相比,EH组和WCH组 PAGTmax、血浆血小板GMP-140含量、MPV均明显增加(P<0.05)而三组血小板计数无统计学差异,同时EH组的PAGTmax、血浆血小板GMP-140含量、MPV均高于WCH组(P<0.05).EH组和WCH组MPV与24 h平均舒张压、GMP-140含量均正相关( P<0.05).结论:WCH存在血小板活化,可能和心血管事件发生率增加有关.     

缬沙坦改善高血压合并糖耐量异常患者内皮功能和炎症因子水平

目的：观察血管紧张素Ⅱ受体拮抗剂缬沙坦治疗对原发性高血压（EH）合并糖耐量异常（IGT）人群血浆一氧化氮（NO）、内皮素（ET）及血浆炎症因子影响。方法：42例EH合并IGT患者口服缬沙坦80mg,1次／d,选择40例正常人作为正常对照组。检测治疗前后血糖,餐后2h血糖（2hPG）,胰岛素抵抗指数（HOMA—IR）,血清炎症因子和NO水平的变化。结果：与正常对照组比较,EH＋IGT组血压、2hPG、HOMA—IR、肿瘤坏死因子α（TNF-α）、白细胞介素6（IL-6）,内皮素水平明显升高,NO水平明显降低（P〈0．01）;与治疗前比较,缬沙坦治疗8周末血压[（163．95±8．0）／（99．10±11．8）mmHg比（132．93±10．7）／（82．14±9．5）mmHg]、2hPG[（9．10±1．10）mmol／L比（7．85±1．15）mmol／L]和HOMA-IR[（3．90±2．11）比（2．73±1．71）]、血浆ET[（47．84±7．79）ng／L比（31．84±4．5）ng／L]、TNF-α[（32．30±5．49）ng／L比（26．83±4．83）ng／L]和IL-6[（112．70±24．79）ng／L比（77．224-11．53）ng／L]水平显著下降,血浆NO显著上升[（38．1±7．36）μmol／L比（43．38±7．52）μmol／L],P均〈0．01。结论：缬沙坦可降低原发性高血压合并糖耐量异常患者血压、血糖、胰岛素抵抗、血浆内皮素、炎症因子水平,升高一氧化氮水平,改善血管内皮功能,抑制炎症反应。     

原发性高血压患者血清脂联素水平与IL-6的相关性

目的:探讨高血压患者血清脂联素(adiponectin,APN)水平,以及APN与白细胞介素-6(interlectin-6,IL-6)的相关性。方法: 选取原发性高血压患者60例(HT组,其中高血压Ⅰ级、Ⅱ级和Ⅲ级患者分别为20例),健康对照者20例(Control组),采用酶联免疫吸附法测定两组患者血清APN水平和IL-6水平。结果: 高血压患者血清APN水平［(8.2±3.8) mg/L］显著低于健康对照组［(10.4±2.9) mg/L］(P<0.05),而IL-6水平［(81±4) μg/L］高于健康对照组［(18±5) μg/L］(P<0.05),APN水平与IL-6呈负相关(r=-0.782,P<0.05)。多元回归分析表明,收缩压、高血压分级和IL-6水平可显著影响原发性高血压患者血清APN水平的变化。结论: 原发性高血压患者存在低脂联素血症,且与高血压严重程度密切相关。     

Increased circulating concentrations of asymmetric dimethylarginine (ADMA) in white coat hypertension

Elevated plasma levels of the endogenous nitric oxide (NO) synthase inhibitor asymmetric dimethylarginine (ADMA) contribute to endothelial dysfunction and seem to be a predictor for cardiovascular mortality. Elevated ADMA plasma concentrations have been demonstrated in patients with hypertension. However, the plasma concentrations of ADMA in white coat hypertension (WCH) has not been previously studied. The aim of this study was to evaluate ADMA in WCH and compare with normotensive (NT) and hypertensive (HT) patients. We also evaluated the relation between ADMA and NO in these three groups. For this purpose, 34 NT, 34 white coat hypertensive (clinical hypertension and ambulatory daytime blood pressure <135/85 mmHg) and 34 HT patients were recruited in this study. The subjects were matched for age, gender, body mass index (BMI) and the patients with smoking habit, dyslipidaemia and diabetes mellitus were excluded. The ADMA levels were determined by high performance liquid chromatography. Plasma ADMA levels were significantly higher in WCH group than in the NT group (3.21+/-0.49 micromol/l vs 2.84+/-0.58 micromol/l, P=0.046). It was significantly higher in the HT group than in the NTs (4.24+/-0.38 micromol/l, P<0.001). There was also a significant difference between the HT and WCH groups (P<0.001). The WCH subjects had significantly higher levels of NO than the HTs (41.68+/-2.23 vs 32.18+/-2.68 micromol/l; P<0.001) and significantly lower values than the NTs (48.24+/-4.29 micromol/l; P<0.001). In WCH and HT group, there was a negative correlation between ADMA and NO (r=-0.515, P=0.003 and r=-0.389, P=0.034, respectively). In NT subjects, there was no correlation between these two parameters (r=-0.287, P=0.124). The correlation between ADMA and NO was stronger in WCH group than in HT group. Although NO levels in HT patients were lower than WCHs and ADMA levels were higher in HT patients than WCHs, the negative correlation of these two parameters were more pronounced in WCH group. Decreased NO and increased ADMA levels in WCH may indicate endothelial dysfunction. Our data indicate also that WCH represent an intermediate group between NT and HT when endothelial dysfunction is concerned.     

白大衣高血压血管紧张素转换酶基因多态性分析

目的：研究白大衣高血压与血管紧张素转换酶（angiotensin converting enzyme，ACE）基因I／D多态性的关系。方法：应用多聚酶链式反应（PCR）方法对白大衣高血压，高血压病Ⅰ级患者和正常血压者各30例进行ACE I／D基因型检测，并分析比较。结果：白大衣高血压和高血压病Ⅰ级组Ⅱ基因型低于正常组（P〈0．01），白大衣高血压和高血压病Ⅰ级组DD基因型高于正常组（P〈0．01），白大衣高血压ID基因型显著高于高血压病Ⅰ级组和正常组（P〈0．01）。高血压病Ⅰ级组ID基因型低于正常组（P〈0．01）。结论：白大衣高血压与ACE基因多态性有关，ID基因型者易患白大衣高血压。     

氯沙坦对高血压左室肥厚患者血浆脑钠肽的影响

目的：研究氯沙坦干预对高血压伴左室肥厚患者脑钠肽（BNP）的影响及意义。方法：选择100例左室射血分数正常范围的高血压患者,其中58例伴左室肥厚,42例不伴左室肥厚,另选50例健康者作为健康对照组,比较三组间血浆BNP水平。左室肥厚组给予氯沙坦治疗6个月,比较治疗前后BNP、左室质量指数（LVMI）的变化。结果：①高血压伴左室肥厚患者BNP浓度显著高于不伴左室肥厚组及健康对照组[（62．21±9．70）pg／ml比（39．35±10．57）pg／ml比（13．89±5．34）pg／ml,P〈0．01];②BNP的浓度与LVMI呈正相关（r=0．44,P〈0．05）;③与治疗前比较,氯沙坦治疗高血压伴左室肥厚6个月后,血浆BNP[（62．21±9．70）pg／ml比（38．78±7．94）pg／m1]、LVMI[（128．71±12．64）g／m。比（107．36±11．32）g／m。]均显著降低（P〈o．01）。结论：氯沙坦可明显降低高血压伴左室肥厚患者脑钠肽水平,逆转左室肥厚。     

血浆同型半胱氨酸与冠心病及高血压的相关性研究

目的探讨冠心病及高血压患者中,血浆同型半胱氨酸、一氧化氮水平的变化。方法对99例冠心病患者(冠心病组)与122例单纯高血压患者(高血压组)进行血浆同型半胱氨酸、一氧化氮水平的测定。结果冠心病组血浆同型半胱氨酸浓度为(18.57±7.47)μmol/L,明显高于高血压组(14.53±10.58)μmol/L(P0.01)。冠心病组血清一氧化氮浓度为(51.15±18.78)μmol/L,明显低于高血压组(70.39±41.55)μmol/L(P0.001)。结论高同型半胱氨酸血症与冠心病的发生有密切关系,并且同型半胱氨酸水平与一氧化氮呈反比,可能同型半胱氨酸水平与血管损伤的严重程度有明显的相关性。     

脂蛋白相关磷脂酶A2与原发性高血压的相关性

目的：研究原发性高血压（EH）患者血清脂蛋白相关磷脂酶A2（Lp-PLA2）水平的变化,探讨其变化在EH中的可能作用。方法：选择EH患者60例,其中高血压1级组患者20例,≥2级组20例,≥2级合并冠心病组20例。另选择健康体检者20例作为正常对照组。用酶联免疫吸附（ELISA）法检测定各组血清Lp-PLA2活性。结果：高血压≥2级合并冠心病组、≥2级组及1级组血清Lp-PLA2水平[（92.53±9.71）μg/L、（86.92±9.61）μg/L、（77.94±8.03）μg/L]均明显高于正常对照组[（71.30±5.99）μg/L],P〈0.05～〈0.01。多元线性逐步回归分析显示血清Lp-PLA2水平与收缩压、舒张压呈正相关（r=0.678,0.503,P均〈0.01）,亦与低密度脂蛋白胆固醇水平呈正相关（r=0.519,P〈0.01）。结论：血清脂蛋白相关磷脂酶A2水平与高血压的严重程度相关,可能参与高血压的发生、发展过程。     

糖代谢异常对原发性高血压患者血管内皮损伤的影响

目的：探讨糖代谢异常对原发性高血压（EH）患者血管内皮损伤的影响。方法：对46例单纯EH患者（EH组）与33例EH合并2型糖尿病（T2DM）患者（EH＋T2DM组）的血糖、血脂、体质指数（BMI）及血清同型半胱氨酸（Hcy）、尿微量白蛋白浓度进行测定、比较,同时分析血清Hcy及尿微量白蛋白浓度与血糖、血脂及BMI之间的相关性。结果：与EH组相比,EH＋T2DM组的BMI、血糖[空腹血糖（FBG）、餐后2h血糖（2hPBG）、糖化血红蛋白（HbAlc）,血脂[甘油三酯（TG）、低密度脂蛋白胆固醇（LDL．C）及载脂蛋白B（ApoB）]水平均显著升高（P〈0．05或〈0．01）,而且血清Hcy[（12．78±2．51）μmol／L比（16．26±2．91）μmol／L]及尿微量白蛋白水平[（19．45±5．24）mg／L比（33．65±10．70）mg／L]升高更加显著（P〈0．01）;Pearson相关分析显示,在EH＋T2DM组患者,血清Hcy水平分别与BMI、FBG、HbAlc、LDL．C、ApoB及尿微量白蛋白水平显著正相关（r=0．667～0．906,P均〈0．01）,而尿微量白蛋白水平则分别与BMI、HbAlc、LDL-C、ApoB及血清Hcy水平显著正相关（r=0．566～0．685,P均〈0．01）。结论：糖代谢异常可加重原发性高血压患者的血管内皮及肾微血管损伤,而且这与血糖代谢异常程度密切相关;控制血糖水平可减轻血管损伤,进而延缓心血管疾病及肾脏并发症的病理进展。     

高血压并糖耐量减低患者肿瘤坏死因子-α和白细胞介素-6的含量及意义

目的：观察原发性高血压（EH）合并糖耐量减低（IGT）患者血浆肿瘤坏死因子α（TNF-α）和白细胞介素-6（IL-6）水平的变化,探讨其与EH合并IGT的关系。方法：入选EH患者82例,分为EH合并IGT组（EH＋IGT组,42例）,EH糖耐量正常组（EH组,40例）,同时随机选择血压正常的健康人40例为健康对照组。检测各组TNF-α、IL-6、空腹血糖（FPG）、餐后2h血糖（2hPG）水平,计算胰岛素抵抗指数（HOMA-IR）。结果：与健康对照组、EH组比较,EH＋IGT组2hPG[（6.50±0.81）mmol/L、（6.59±0.79）mmol/L比（9.10±1.10）mmol/L]、HOMA-IR[（1.25±0.64）、（1.93±1.05）比（3.90±2.11）]明显升高（P均〈0.01）;与健康对照组比较,EH组、EH＋IGT组血浆TNF-α[（23.83±2.28）ng/ml比（27.80±4.73）ng/ml比（32.30±5.49）ng/ml]、IL-6[（76.76±12.81）ng/ml比（90.62±18.09）ng/ml比（112.97±24.88）ng/ml]水平明显升高（P〈0.05～0.01）,且EH＋IGT组明显高于EH组的（P均〈0.05）。多因素Logistic回归分析显示,EH合并IGT与TNF-α、IL-6、FPG、2hPG呈正相关（β为1.247,1.180,0.516,0.140;P〈0.05～0.01）。结论：原发性高血压合并糖耐量减低患者血浆肿瘤坏死因子α、白细胞介素6水平升高,提示其体内炎症反应增强。     

赖诺普利、氨氯地平和比索洛尔对高血压病患者血浆一氧化氮、前列环素与内皮素的影响

目的：探讨高血压病患者血浆一氧化氮（ Ｎ０）,前列环素（ Ｐ Ｇ Ｉ２ ）与内皮素（ Ｅ Ｔ）水平变化及赖诺普利、氨氯地平、比索洛尔对这些物质的影响。　方法：测定２０ 名正常人、８４ 名高血压病患者的血浆硝酸盐和亚硝酸盐（ Ｎ Ｏ 的代谢产物）、６┐酮┐前列腺素 Ｆ１α（ Ｐ Ｇ Ｉ２ 代谢产物）、 Ｅ Ｔ水平与血压,并进行治疗前后的对比分析。４６ 名患者用赖诺普利治疗,２０ 名用氨氯地平治疗,１８ 名用比索洛尔治疗,疗程均为８ 周。　结果：患者血浆 Ｎ Ｏ 和 Ｐ Ｇ Ｉ２ 水平明显低于正常人,而 Ｅ Ｔ水平显著高于正常人。这种变化与病情严重程度相平衡。赖诺普利组治疗后各期 Ｎ Ｏ、 Ｐ Ｇ Ｉ２ 水平提高, Ｅ Ｔ水平下降。氨氯地平组治疗后 Ｅ Ｔ水平下降,但 Ｎ Ｏ、 Ｐ Ｇ Ｉ２ 水平无改变。比索洛尔组治疗后 Ｎ Ｏ、 Ｐ Ｇ Ｉ２、 Ｅ Ｔ均无显著改变。　结论：高血压病与血浆 Ｎ Ｏ、 Ｐ Ｇ Ｉ２ 水平呈负相关,而与 Ｅ Ｔ水平呈正相关,此现象随着病情加重而更显著。赖诺普利组治疗后其疗效与 Ｎ Ｏ、 Ｐ Ｇ Ｉ２ 水平呈正相关,而与 Ｅ Ｔ水平呈负相关,这可能是 Ａ Ｃ Ｅ Ｉ赖诺普利的降压机理之一。     

Endothelium and angiogenesis in white coat hypertension

Hypertensive patients are at particular risk of cardiovascular complications, possibly related to endothelial damage or dysfunction, or to abnormal angiogenesis. The aim of this study was to compare the risk conferred by white coat hypertension (WCH) vs sustained hypertension in the development of the endothelial dysfunction and abnormal angiogenesis by evaluating nitric oxide (NO=NO2+NO3), endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), and E-selectin levels in plasma. The study group included 102 subjects, 34 with WCH (17 male and 17 female patients) aged 49+/-11 years, 34 sustained hypertensives (HT) (15 male and 19 female patients) aged 47+/-11 years and 34 normotensive control subjects (NT) (16 male and 18 female patients) aged 48+/-10 years. WCH was defined as clinical hypertension and daytime ambulatory blood pressure less than 135/85 mmHg. The subjects were matched for age, gender, body mass index and the patients with smoking habit, dyslipidaemia, and diabetes mellitus were excluded from the study. The NO, ET-1, VEGF and E-selectin levels were analysed by ELISA technique. The WCH subjects had significantly higher levels of NO than the HT (41.68+/-2.23 vs 32.18+/-2.68 micromol/l; P<0.001) and significantly lower values than the NT (48.24+/-4.29 micromol/l; P<0.001). ET-1 levels of the WCH group were significantly higher than the NT (8.10+/-0.92 vs 5.95+/-0.26 ng/ml; P<0.001) and significantly lower than the HT (11.46+/-0.59 ng/ml; P<0.001). Considering with VEGF, the WCH group had significantly higher levels than the NT (195.88+/-11.84 vs 146.26+/-18.67 pg/ml; P<0.001), but the difference from the HT group was not significant (203.35+/-7.48 pg/ml; P=0.062). E-selectin in the WCH group was significantly lower than the HT (4.77+/-0.52 vs 8.49+/-2.85; P<0.001), but the difference from the NT group was not significant (3.86+/-0.67; P=0.077). Our data demonstrate that WCH is associated with endothelial dysfunction and abnormal angiogenesis. The degree of these changes is not as severe as observed in hypertensive population.     

高血压左室肥厚患者血浆sTRAIL、sDR4、sDR5水平的变化(英文)

目的:测定高血压左室肥厚患者血浆肿瘤坏死因子相关的凋亡诱导配体(sTRAIL)、及其死亡受体(sDR4、sDR5)水平。方法:用酶联免疫吸附法(ELISA)分别检测50例高血压左室肥厚患者(高血压左室肥厚组)、50例高血压无左室肥厚患者(高血压组)和50例健康人(健康对照组)血浆sTRAIL、sDR4和sDR5水平。结果:①与健康对照组及高血压组比较,高血压左室肥厚组血浆sTRAIL[(0.95±0.11)ng/ml比(1.12±0.86)ng/ml比(1.74±1.19)ng/ml]、sDR4[(2.38±0.32)pg/ml比(5.63±1.05)pg/ml比(8.72±1.14)pg/ml]、sDR5[(<6 pg/ml)比(39.19±8.23)pg/ml比(78.21±11.2)pg/ml]水平均明显升高(P<0.01);且高血压组sDR4、sDR5水平明显高于健康对照组(P<0.01),sTRAIL水平与健康对照组无明显差异(P>0.05);②Pear-son相关分析表明,高血压左室肥厚患者sTRAIL、sDR4、sDR5间呈显著的正相关性(r=0.325～0.410,P<0.05或<0.01)。结论:血浆sTRAIL、sDR4、sDR5水平可能是预测高血压患者左室肥厚有价值的指标之一。     

冠心病合并糖尿病患者冠状动脉狭窄程度与内皮功能损伤的相关性研究

目的：探讨冠心病（CHD）合并2型糖尿病（DM）患者冠状动脉狭窄与内皮功能损伤的相关性。方法选择行冠状动脉造影确诊的CHD患者86例,其中46例合并2型DM（DM组）、40例为非糖尿病患者（NDM组）。用Gensini积分法评估冠状动脉狭窄程度;硝酸还原酶法比色检测患者血浆一氧化氮（NO）浓度;ELISA法测定血浆内皮素（ET）,血管性血友病因子抗原（vWF：Ag）、血小板膜蛋白-140（GMP-140）浓度;发光底物法测定血浆组织型纤溶酶原激活剂（t-PA）与血浆纤溶酶原激活物抑制剂-1（PAI-1）活性以评价内皮功能损伤情况。采用直线相关分析法对DM患者Gensini积分与内皮损伤相关指标进行分析。结果 DM组患者的Gensini积分明显大于NDM组（38.25±12.13vs.28.73±10.74,P＜0.05）;DM组患者的NO、t-PA水平明显低于NDM组[NO：（52.35±17.62）μmol/Lvs.（98.37±21.20）μmol/L;t-PA：（0.55±0.21）IU/Lvs.（0.87±0.26 IU/L）;P＜0.01];而ET、PAI-1、vWF：Ag、GMP-140水平明显高于NDM组。DM组患者血浆NO（r=-0.803）、t-PA水平（r=-0.628）与Gensini积分呈显著负相关（P均＜0.01）,而ET（r=0.713）、PAI-1（r=0.526）、vWF：Ag（r=0.705）和GMP-140（r=0.512）与Gensini积分呈显著正相关（P均＜0.01）。结论 CHD合并DM患者的Gensini积分与内皮损伤程度密切相关。严重的内皮功能损伤可能是DM患者冠状动脉狭窄程度较重的原因之一。     

关于高血压患者血清HGF、sICAM-1水平的研究（英文）

目的：探讨高血压患者血清肝细胞生长因子（HGF）,可溶性细胞间黏附分子-1（sICAM-1）水平的变化及其意义。方法：选择59例高血压患者,其中高血压1级组20例,高血压2级组19例,高血压3级组20例,并选择30例健康体检者作为正常对照组。用酶联免疫双抗体夹心法检测各组血清HGF和sICAM-1浓度,并进行比较。结果：与正常对照组相比,高血压患者血清HGF[（641.65±142.90）pg/ml比（998.15±241.38）pg/ml]、sI-CAM-1[（161.70±32.36）ng/ml比（327.17±31.28）ng/ml]水平明显升高（P〈0.01）,血压越高,其变化越显著（P〈0.01）,HGF浓度与sICAM-1浓度呈正相关（r=0.317,P〈0.01）。结论：HGF与sICAM-1可能参与了高血压的发病过程,而且HGF在高血压内皮细胞损伤的修复中可能具有重要作用。     

气体信号分子NO和CRP在脑血管性疾病及血管性痴呆患者血浆中的变化和意义

目的探讨血管性痴呆、脑血管疾病患者血浆中一氧化氮(NO)和C反应蛋白(CRP)水平变化及可能的临床意义。方法 1.收集脑血管疾病患者40例、血管性痴呆患者46例,正常对照50例。全部研究对象均应用简明精神状态量表、日常生活能力量表、Hachinski缺血指数和Hamilton抑郁量表量表进行检测,血管性痴呆患者用全面衰退量表分级。取空腹静脉血2ml,迅速分离血浆并置于-70℃冰箱保存。2.NO和CRP分别以硝酸还原酶法及散射比浊法进行测定。结果 1.NO水平:血管性痴呆组为39.84±17.28μmol/L、脑血管疾病组为42.72±17.19μmol/L,均较对照组的62.92±17.58μmol/L明显降低(P0.01);病例组之间差异无统计学意义(P0.05)。相关分析显示血浆NO水平与血管性痴呆患者痴呆的严重程度没有相关性。2.CRP水平:血管性痴呆组(5.26±3.47mg/L)和脑血管疾病组(3.01±1.78mg/L)较对照组(1.36±1.33mg/L)升高(P0.05),且血管性痴呆组血浆CRP水平明显高于脑血管疾病组(P0.05)。血浆CRP水平与血管性痴呆的严重程度呈正相关。3.各组内NO与CRP的相关分析显示:各组内NO与CRP血浆水平没有明显的相关性。结论 1.气体信号分子NO在血管性痴呆及脑血管疾病患者中水平降低,但与血管性痴呆患者痴呆的严重程度没有相关性;2.血管性痴呆和脑血管疾病患者CRP升高提示炎症可能参与了脑卒中的发病。     

Serum gamma-glutamyl transferase (GGT) levels and inflammatory activity in patients with non-dipper hypertension

Non-dipper hypertension is associated with increased cardiovascular morbidity and mortality. We aimed to evaluate serum gamma-glutamyl transferase (GGT) level, which is accepted as a marker for oxidative stress and its relationship with inflammatory activity in patients with non-dipper hypertension. Age and sex matched 43 dipper hypertensive patients, 40 non-dipper patients, and 46 healthy subjects were included into the study. Serum GGT and C-reactive protein (CRP) levels were measured and compared between each of the groups. Serum GGT activity was higher in the non-dipper and the dipper hypertensive groups than in the control group (33.5 ± 11.8 and 28.1 ± 10.1 U/l, respectively, vs. 21.2 ± 6.5 U/l; p < 0.001). There was a statistically significant difference in serum GGT activity between the non-dippers and the dippers (p = 0.021). When compared with the control group, serum CRP levels were significantly increased in both the non-dipper and the dipper hypertensive groups (6.1 ± 2.6 and 5.4 ± 2.1 mg/l, respectively, vs. 2.8 ± 1.7 mg/L; p < 0.001). Increased CRP levels were higher in non-dippers than dippers (p = 0.046). A significant correlation was found between GGT and CRP measurements (r = 0.37, p = 0.002). Serum GGT levels, which are markers of the oxidative stress and CRP levels, are both increased in non-dipper hypertension. Increased GGT activity, found to be correlated with CRP levels, may be one of the reasons behind the non-dipper hypertension related cardiovascular complications.     

白介素-7与原发性高血压血管内皮生长因子的相关性研究

目的：探讨白介素-7（IL-7）与原发性高血压血管内皮功能改变之间的关系。方法：50例实验组分为高血压病1级组25例，高血压病合并冠心病组25例。另设正常对照组20例。使用酶联免疫吸附法进行各组血清IL-7与血管内皮生长因子（VEGF）浓度测定，同时测定血糖、血脂，比较各组间检测指标的差异。结果：（1）高血压组血清IL-7含量（105．30土15．77）pg／ml及VEGF含量（13．58±3．55）ng／ml均高于正常对照组IL-7含量（70．14±6．45）pg／ml及VEGF含量（2．58±0．66）ng／ml（P均〈0．01）；（2）高血压病合并冠心病组，血清IL-7含量（119．62±6．41）pg／ml与VEGF含量（16．18±2．57）ng／ml，均高于高血压病1级组的IL-7（90．91±4．89）pg／ml与VEGF（6．98±2．25）ng／ml，以及正常对照组（P均〈0．01）；（3）高血压病1级组、高血压合并冠心病组的VEGF水平与IL-7浓度呈正相关（r=0．481，P〈0．05；r=0．558，P〈0．01）结论：血清IL-7水平升高与VEGF水平升高呈正相关，可能参与了原发性高血压的发生、发展。     

原发性高血压患者血压变异性与早期肾功能损害的相关性研究

目的：观察原发性高血压（EH）患者血压变异性与尿微量白蛋白/尿肌酐比值的相关性。方法：随机选择60例EH患者作为EH组,按照24h平均动脉压均值高度又分为3个亚组,即EH1组（90.2～106.6mmHg）、EH2组（106.6～118.3mmHg）及EH3组（118.3～143.7mmHg）,各亚组均20例,另选择15例健康正常人作为健康对照组。监测所有研究对象在日间、夜间及24h收缩压变异性和舒张压变异性,以晨尿微量白蛋白/尿肌酐比值作为早期肾功能损害的指标,研究其相关性。结果：两组均存在血压变异性,与健康对照组比较,EH组日间、夜间及24h收缩压变异性[日间：（12.62±2.96）比（17.62±3.27）,夜间：（8.32±2.14）比（11.63±2.35）,24h：（11.23±2.25）比（18.35±2.94）]和舒张压变异性[日间：（10.32±2.41）比（12.48±2.85）,夜间：（9.52±2.00）比（11.59±3.12）,24h：（10.68±2.16）比（13.45±3.00）]均明显增大（P均〈0.01）。双变量相关分析显示EH组及EH各个亚组的日间、夜间及24h收缩压和舒张压的血压变异性均与尿微量白蛋白/尿肌酐比值均呈正相关（r=0.217～0.485,P〈0.05）。结论：原发性高血压患者血压变异性与早期肾脏损伤密切相关,改善血压变异性对预防早期肾功能损害有益。