高血压患者血肝细胞生长因子与血管内皮功能的关系及干预研究

目的 研究高血压患者血清肝细胞生长因子(HGF)与血管内皮功能不全的相关性;氯沙坦/氢氯噻嗪复方片(海捷亚)是否可降低高血压患者血清HGF水平和改善血管内皮功能.方法 高血压(HT)患者70例,包括1级高血压(HT1组)患者27例、2级高血压(HT2组)患者31例、3级高血压(HT3组)患者12例.选择其中30例HT患者行海捷亚干预治疗.20例健康体检者为正常对照组.分别测定基线及海捷亚治疗后血清HGF、血浆内皮素(ET)和血清一氧化氮(NO)水平.结果 1) 血HGF和ET水平:HT3组高于HT2组、HT1组和对照组(P均＜0.05),HT2组和HT1组高于对照组(P均＜0.05),HT2组和HT1组之间无显著性差异(P值分别为0.061和0.162);血清NO水平:HT各组均低于对照组,且随着血压级别的增高而降低(P均＜0.05);2)相关分析结果显示:血清HGF与NO呈负相关、与ET呈正相关(相关系数分别为-0.633、0.741,P值均＜0.01);3)海捷亚治疗8周后血清HGF和ET明显降低,而血清NO明显增高(P值均＜0.01).结论 1)高血压患者血清HGF增高,其水平可能反映了血管内皮功能不全的严重程度;2)高血压患者应用海捷亚治疗后血清HGF水平下降、血管内皮功能改善.     

高血压患者血清肝细胞生长因子水平与血管内皮功能的关系及坎地沙坦酯的干预效果

目的探讨高血压患者血清肝细胞生长因子(HGF)水平与血管内皮功能的关系及坎地沙坦酯的干预效果。方法选择该院心血管内科2013年10月至2014年12月收治的高血压患者60例为病例组,同时选取30例健康体检者(血压正常)为对照组,检测血清HGF、内皮素(ET)、一氧化氮(NO)指标,分析血清HGF水平与血管内皮功能的关系及坎地沙坦酯的干预效果。结果病例组中随着病情加重HGF、ET-1水平逐渐升高,NO水平逐渐降低(P0.05);病例组各级别中NO、ET-1、HGF水平与对照组相比差异显著(P0.05)。病例组干预前经过检测HGF、NO、ET-1水平分别为(1 543.23±24.67)pg/ml、(12.38±2.36)μmol/L、(89.90±14.38)ng/L;HGF水平与NO呈负相关(r=-0.456,P=0.005),与ET-1呈正相关(r=0.765,P=0.001)。干预12 w后HGF与ET-1水平明显降低,NO水平明显升高,与干预前相比均具有统计学差异(P0.05)。结论高血压患者血清HGF明显升高,HGF水平变化与血管内皮功能密切相关,坎地沙坦酯干预后HGF水平下降,改善了血管内皮功能。     

高血压患者血清肝细胞生长因子的表达及与血管内皮功能的关系

目的探讨高血压患者血清肝细胞生长因子(HGF)的表达及与血管内皮功能的关系。方法 60例高血压患者,按血压高低分级分为轻度组(n=21)、中度组(n=27)及重度组(n=12),另选取30例健康体检者作为对照组,比较各组受试者基线指标及HGF、血浆内皮素(ET)及血浆一氧化氮(NO)水平,同时分析HGF水平与ET及NO的相关性。结果各组受试者性别、年龄、空腹血糖(FBG)、甘油三酯(TG)比较差异无统计学意义(P>0.05)。各组高血压患者血清HGF、ET及NO水平与对照组差异显著(P<0.05);HGF及ET水平随血压的增高而增高,NO水平随血压的增高而下降,重度组各指标与轻度组及中度组差异显著(P<0.05);轻度组与中度组HGF及NO水平差异显著(P<0.05)。Spearman相关性分析显示,HGF与ET水平呈显著正相关(r=0.69,P<0.05),HGF与NO水平呈显著负相关(r=-0.60,P<0.05)。结论高血压患者血液中HGF的水平与血压水平及机体血管内皮功能受损程度具有显著相关性,可作为反映高血压患者内皮功能受损程度的一个新指标。     

高血压患者颅底血流速度改变与内皮素、一氧化氮关系的探讨

目的　研究血管内皮细胞合成分泌的血管活性物质内皮素 (ET)、一氧化氮 (NO)与高血压患者脑血流改变的关系。方法　测定 5 4例高血压患者与 2 0例非高血压患者血浆ET及NO水平 ,同时测定经颅多普勒血流。结果　①高血压组的颅底动脉收缩期峰值流速 (VS)及脉动指数(PI)明显高于对照组 (P <0 .0 5 ) ;②高血压病人血浆NO与颅底动脉血流速度呈负相关 (P <0 .0 2 ) ,ET与颅底动脉血流速度呈正相关 (P <0 .0 1) ;③高血压组血浆NO水平明显低于对照组 (P <0 .0 5 ) ,ET水平高于对照组 (P <0 .0 5 ) ,中重度高血压组NO水平低于轻度高血压组 (P <0 .0 5 ) ,ET水平高于轻度高血压组 (P <0 .0 5 )。结论　血浆ET和NO水平在一定程度上反映了高血压及其血管内皮损伤的程度     

2型糖尿病患者血清肝细胞生长因子变化与血管内皮功能的关系

目的探讨2型糖尿病（T2DM）患者血清肝细胞生长因子（HGF）变化与血管内皮功能的相关性。方法将40例T2DM患者分为单纯T2DM（A组）及伴血管病变T2DM（B组）各20例,检测其血清HGF、血浆内皮素（ET）、血清NO及糖脂代谢指标;并与20例体检健康者（对照组）进行比较。结果与对照组比较,A、B组血清HGF、ET升高,NO降低（P〈0．05或〈0．01）,B组异常程度更高（P〈0．05）;血清HGF水平与患者的收缩压、空腹血糖、糖化血红蛋白、LDL-C、ET呈正相关（r分别为0．54、0．53、0．59、0．71、0．67,P均〈0．01）,与NO及HDL-C呈负相关（r分别为-0．54、-0．63,P均〈0．01）。结论T2DM患者血清HGF明显升高,其可能反映血管内皮功能损伤的严重程度。     

高血压患者血管内皮功能的改变及氯沙坦的影响

目的:评价高血压患者血管内皮功能的改变及氯沙坦的影响。方法:随机选择原发性高血压患者40例,检测其内皮素(ET)、心钠素(ANP)和一氧化氮(NO)水平的变化。结果:与正常对照组比较,高血压组患者ET、ANP水平上升明显(P均<0.05),NO水平明显下降(P<0.05),氯沙坦治疗后ET水平无明显变化,ANP下降明显(P<0.05),NO水平上升明显(P<0.05)。结论:高血压患者血管内皮功能有明显变化.氯沙坦不仅有较好的降压作用,可能也有较好的血管内皮保护功能。     

原发性高血压患者血清过氧化氢酶的变化以及海捷亚的干预效果

目的:观察原发性高血压患者血清过氧化氢酶(CAT)的变化以及海捷亚的干预效果。方法:选择原发性高血压患者60例,随机分为海捷亚组30例(海捷亚每日1次,每次1片,无效者2周后改为2片)和对照组(非洛地平2.5mg,每日1次,无效者2周后改为5mg)30例,治疗4周,分别检测治疗前后患者平均动脉压和血清CAT的活力变化。结果:治疗前两组平均动脉压无显著性差异(P>0.05),治疗后两组的平均动脉压均较治疗前下降(P均<0.05),但海捷亚组治疗前后差值较对照组高,有显著性差异(P<0.05)。治疗前两组血清中CAT活力无显著性差异(P>0.05),治疗后两组血清中CAT的活力均较治疗前增加(P均<0.01),但海捷亚组血清CAT治疗前后差值较对照组高,有极显著性差异(P<0.01)。结论:海捷亚除对原发性高血压患者具有良好的降压效果外,还能够增加患者的CAT活力,清除过多的氧自由基,防止血管内皮细胞的脂质过氧化。     

阻塞性睡眠呼吸暂停综合征老年患者血管内皮功能变化及其与冠心病的关系

目的　探讨老年阻塞性睡眠呼吸暂停综合征 (OSAS)患者血管内皮功能变化与冠心病的相关性。　方法　选择中、重度OSAS患者 4 7例为OSAS组 ,又分伴冠心病 (18例 )和不伴冠心病(2 9例 )两亚组 ;另选 17例单纯冠心病患者和健康老年人 31例作为对照组。比较各组间血浆一氧化氮 (NO)、内皮素 (ET)和NO/ET的动态变化。　结果　与对照组比较 ,OSAS两组及单纯冠心病组患者NO水平降低 ,ET水平增高 ,NO/ET比值下降 (均为P <0 0 5 ) ,而OSAS伴冠心病者下降更明显。OSAS不伴冠心病者的NO、ET水平及NO/ET比值与单纯冠心病组比较 ,差异无显著性 ,OSAS伴冠心病者的NO和ET水平亦无显著性差异 ,但NO/ET值下降已有统计学意义 (P <0 0 5 )。　结论　OSAS老年患者存在明显血管内皮功能障碍 ,尤以伴冠心病者为甚 ,血管内皮功能损伤可能是OSAS患者并发冠心病的原因之一     

原发性高血压患者肝细胞生长因子、血管紧张素Ⅱ、内皮素的变化及苯那普利的干预作用

目的:探讨原发性高血压(EH)患者血清肝细胞生长因子(HGF)及血管紧张素Ⅱ(AngⅡ)、内皮素(ET)的浓度与原发性高血压进展的关系及苯那普利对其生成的影响.方法:以20例健康人做对照(正常对照组),另选择1、2级原发性高血压患者40例(为1级原发性高血压组18例,2级原发性高血压组22例),分别采用酶联免疫吸附法和放射免疫法测定苯那普利治疗前及治疗6周后血清中HGF、AngⅡ和ET浓度.结果:1、2级原发性高血压组治疗前血清HGF、ET和AngⅡ水平明显高于正常对照组(P＜0.05～0.01);并与平均动脉压呈正相关(r分别为0.568、0.460、0.623);血清HGF与ET、AngⅡ亦有良好相关性(r分别为0.512、0.563).治疗后血压下降,同时血清HGF、ET和AngⅡ水平较治疗前明显下降(P＜0.05).结论:HGF、AngⅡ及ET水平与高血压有关.苯那普利在降压的同时能降低HGF及AngⅡ、ET水平.     

原发性高血压患者血清肝细胞生长因子的测定

目的 :肝细胞生长因子 (HGF)是一种特异性内皮生长因子 ,参与血管内皮损伤修复过程。高血压引起的血管内皮细胞损伤也可能导致HGF异常 ,为研究这一可能性 ,本项目测定无肝肾功能损伤及其他并发症的原发性高血压患者及正常对照者的血清HGF浓度。方法 :18例男性高血压患者及 13例男性正常对照者入选。所有受试者停药二周。血清HGF浓度用酶联免疫分析法(ELISA)测定。结果 :正常对照组血清HGF浓度为 0 32 1± 0 12 5ng/ml;原发性高血压组为 0 36 8± 0 2 6 9ng/ml,二组之间无显著性差异 (P >0 0 5 )。收缩压 ,舒张压及平均动脉压与血清HGF水平无相关性。结论 :血清HGF在轻 ,中度原发性高血压患者中并不增高。高血压引起血管内皮细胞损伤时 ,虽然局部HGF迅速产生 ,但循环HGF并不受影响。     

血清肝细胞生长因子在慢性肝病中的意义

目的 肝细胞生长因子(HGF)能促进上皮细胞增生、运动、变形，是肝再生的起始因子之一，近来发现其在肝硬化和肝肿瘤的发生发展中也有重要作用。现主要探讨血清HGF水平在慢性肝病中的意义。方法 检测197例个体血清HGF水平，包括肝细胞癌(HCC)80例，肝硬化(LC)57例，慢性肝炎(CH)22例，正常对照38例。ELISA法检测血清HGF水平，并描绘受试者工作曲线(ROC)，确定HCC和LC患者HGF水平的最佳临界点。运用Spearman相关分析HGF水平和ALT、AST、GGT、白蛋白、总胆红索、凝血时间、肝癌大小、病理分级的相关性。结果 HCC、LC、CH和正常对照组的血清HGF中位值分别是6．767、151．200、7．017和3．476pg／m1。其中HCC组(P＜0．05)和比组(P＜0．01)的血清HGF水平显著高于正常对照组。LC组根据Child分级分层发现，Child C级患者的HGF水平明显高于Child A、B级。肝硬化ROC曲线显示，14pg／m1为临界值时效率最高。血清HGF水平仅发现与凝血时间有相关性(r=0．45，P＜0．01)。在HCC组中，未发现血清HGF水平与肿瘤大小、病理分级有任何相关。结论 血清中HGF水平增高与LC程度有关。     

原发性高血压患者血一氧化氮及内皮素水平的研究

目的 研究原发性高血压患者血一氧化氮（NO）及内皮素（ET）水平的变化与高血压轻重程度、血压节律异常的相关性及其临床意义.方法 高血压组232例,对照组130例.高血压组内分为低危、中危、高危组分别89、78、65例;按血压节律性分为杓型与非杓型组分别109、123例.所有受试者进行NO、ET检测和动态血压分析.结果 高血压组与正常对照组比较血NO降低而ET升高,二者比值下降更明显,在两组间如上三组数据差异均有统计学意义.原发性高血压各组随高血压危险度上升,NO降低,ET升高,二者比值下降的幅度有加大趋势.原发性高血压患者随着正常血压节律性的丧失,NO降低,ET升高,二者比值下降的幅度有加大趋势.结论 血NO上升、ET下降及二者比值的相应明显变化不仅与原发性高血压的发病有关,也与高血压的危险程度和血压正常节律的存在与否具有明显的相关性.     

缬沙坦联合氨氯地平或氢氯噻嗪对老年高血压患者血压变异性的影响

目的 比较缬沙坦联合氨氯地平或氢氯噻嗪对老年高血压患者血压变异性及一氧化氮、内皮素的影响.方法选取61例2、3级老年高血压患者,随机分为两组,分别给予缬沙坦+氨氯地平或缬沙坦+氢氯噻嗪行降压治疗,观察入选时、治疗第8周和第16周各种相关指示的变化.人选时检测血脂、空腹血糖、血尿酸,试验各个阶段监测24 h动态血压,检测血浆一氧化氮、内皮素水平.结果在患者入选时、治疗第8周和第16周三个时间点,缬沙坦+氨氯地平组和缬沙坦+氢氯噻嗪组24 h血压及白昼血压比较差异无统计学意义.治疗第16周,缬沙坦+氨氯地平组晨峰收缩压较缬沙坦+氢氯嚷嗪组明显降低[(22.6±8.8)mm Hg(1 mm Hg=0.133 kPa)比(26.3±13.7)mm Hg,P＜0.05];缬沙坦+氨氯地平组及缬沙坦+氢氯噻嗪组24 h收缩压变异性(SBPV)进行性降低[缬沙坦+氨氯地平组:(12.5±2.8)mm Hg比(10.2 ±2.2)mm Hg比(8.8±1.6)mm Hg,P＜0.01;缬沙坦±氢氯噻嗪组:(12.5±2.5)mmHg比(10.7±2.2)mm Hg比(9.6±2.0)mmHg,P＜0.01],缬沙坦+氨氯地平组及缬沙坦+氢氯噻嗪组白昼SBPV明显降低[缬沙坦+氨氯地平组:(12.2±3.0)mm Hg比(10.1±2.3)mm Hg比(8.4±1.9)mm Hg,P＜0.01;缬沙坦+氢氯噻嗪组:(11.8±2.7)mm Hg比(10.4±1.9)mm Hg比(9.6±2.2)mm Hg,P＜0.01],缬沙坦+氨氯地平组24 h舒张压变异性(DBPV)显著降低[(15.5±3.4)mm Hg比(13.0±3.5)mm Hg比(12.3±2.5)mm Hg,P＜0.01],缬沙坦+氢氯噻嗪组24 h DBPV无显著性变化;缬沙坦+氨氯地平组第16周白昼SBPV低于缬沙坦+氢氯噻嗪组[(8.4±1.9)mm Hg比(9.6 ±2.2)mm Hg,p＜0.05],缬沙坦+氨氯地平第8周、第16周的24 h DBPV、白昼DBPV低于缬沙坦+氢氯噻嗪组(P ＜0.01～0.05);缬沙坦+氨氯地平组一氧化氮进行性升高[(27.3±13.6)μmol/L比(47.2±16.3)μmol/L比(69.5±18.9)μmol/L,P＜0.01]、内皮素进行性降低[(45.3±8.0)ng/L比(37.4±3.9)ng/L比(34.2±4.4)ng/L,P＜0.01];缬沙坦+氢氯噻嗪组一氧化氮进行性升高[(33.5±13.9)μmol/L 比(49.7±21.9)μmol/L比(66.7 ±24.7)μmol/L,P＜0.01]、内皮素显著降低[(46.6±10.4)ng/L比(37.0±5.4)ng/L比(36.1±8.2)ng/L,P＜0.01].治疗第8周,缬沙坦+氨氯地平组收缩压变异性的降幅与一氧化氮的升幅有相关性(r =0.401,P=0.025).结论缬沙坦联合氨氯地平或氢氯噻嗪均能降低老年高血压患者血压变异性、改善血管内皮功能,缬沙坦联合氨氯地平可能更适合于老年高血压患者.     

Relationship between hypertensive left ventricular hypertrophy and levels of endothelin and nitric oxide.

To investigate the relationship between hypertensive left ventricular hypertrophy (LVH) and levels of endothelin (ET) and nitric oxide (NO), and to provide an experimental basis for prevention and treatment of hypertensive LVH. Fifty eight hypertensive patients and 14 healthy controls were studied. All patients were examined by echocardiography. Left ventricular mass (LVM) and left ventricular mass index (LVMI) were calculated using Devereux RB formula. Hypertensive patients were divided into a LVH (+) group (n= 21) and a LVH (-) group (n=37), and the levels of endothelin and nitric oxide in the peripheral venous blood were measured. The mean ET level was significantly higher in the LVH (+) group than in LVH (-) group (p < 0.05), but the NO level was significantly lower in the LVH (+) group. The ET/NO ratio was significantly higher in the LVH (+) group than in LVH (-) group (p< 0.01). For the stepwise multiple regression analysis, the LVMI of hypertensive patients served as a dependent variable, and age, sex, BMI, MAP, ET, NO, and ET/NO served as independent variables. Only MAP, ET, and NO were found to have significant correlation to hypertensive LVH. ET had a significant positive correlation, and NO a significant negative relation to LVMI, but ET/NO showed no correlation to hypertensive LVH. ET and NO are involved in hypertensive LVH; the independent action of ET and NO in the pathogenesis of hypertensive LVH may weaken the relation between ET/NO and hypertensive LVH.     

强离子隙在慢性心力衰竭患者中的水平改变及临床意义

目的探讨强离子隙(SIG)水平在慢性心力衰竭(CHF)患者中的改变及其与CHF患者心功能、N末端B型利钠肽前体(NT-proBNP)水平的相关性。方法选择CHF患者90例,根据心功能(NYHA)分级分为心功能Ⅱ级组30例、心功能Ⅲ级组30例和心功能Ⅳ级组30例;根据CHF病因分为冠心病组25例、高血压性心脏病组45例和扩张型心肌病组20例;选择健康体检者35例作为对照组,在测定血气、电解质等的基础上,应用Stewart-Figge方法学的方程式计算SIG,采用电化学免疫法测定NT-proBNP。结果与对照组比较,心功能Ⅱ、Ⅲ和Ⅳ级组患者SIG[(5.54±2.23)mmol/L、(7.65±3.12)mmol/L和(10.54±3.84)mmol/L vs(1.70±0.81)mmol/L]、NT-proBNP[(114.85±36.23)ng/L、(476.30±79.45)ng/L和(782.50±99.38)ng/L vs(42.74±11.29)ng/L]水平明显升高;且心功能Ⅱ、Ⅲ和Ⅳ级组间SIG水平比较,差异有统计学意义(P<0.05)。与治疗前比较,不同心功能组治疗后SIG和NT-proBNP水平明显下降,差异有统计学意义(P<0.01)。GHF患者SIG与NT-proBNP呈正相关(r=0.424,P<0.01)。结论 CHF患者血清SIG水平明显升高,且随着心功能不全程度的加重而升高,与NT-proBNP存在一定的相关性,对CHF的早期诊断、风险评估及治疗评价均具有指导意义。     

Differential effects of strict blood pressure lowering by losartan/hydrochlorothiazide combination therapy and high-dose amlodipine monotherapy on microalbuminuria: the ALPHABET study

We investigated the effects of losartan/hydrochlorothiazide (HCTZ) fixed combination therapy and high-dose amlodipine monotherapy on BP measurements and target organ protection. In this open-label multicenter trial, hypertensive patients were randomly allocated to receive losartan 50 mg or amlodipine 5 mg for 4 weeks, and the treatments were changed to combination of losartan 50 mg/HCTZ 12.5 mg or amlodipine 10 mg for a further 4 weeks. A total of 91 hypertensive patients (age 63.6 years), 47 in the losartan/HCTZ group and 44 in amlodipine group, were enrolled. After 8 weeks, the clinic BP, home BP, and 24-hour ambulatory BP were successfully controlled to the same level in both treatment groups (P < .001). Furthermore, both groups showed the same degree of BP reduction in the 24-hour, daytime, and nighttime (P < .001). B-type natriuretic peptide (BNP) also significantly decreased to the same level in both groups, whereas the reduction of urinary albumin/creatinine ratio (UACR) was greater in the losartan/HCTZ group than in the high-dose amlodipine group (–47.6% vs 2.4%, P < .001). Losartan/HCTZ combination and high-dose amlodipine have similar effects on clinic, home, and ambulatory BP control and BNP reduction, whereas losartan/HCTZ has superior effect on UACR reduction when compared with high-dose amlodipine.     

Effects of losartan on serum total and high-molecular weight adiponectin concentrations in hypertensive patients with metabolic syndrome

High-molecular weight (HMW) adiponectin may have the most biologic activity among several isoforms. We investigated long-term effects of losartan on serum concentrations of total and HMW adiponectin in hypertensive patients with metabolic syndrome (MS) by serial measurements over 6 months. Forty hypertensive patients first received 50 mg of losartan. Upward titration of the losartan dose was implemented to reach a target blood pressure of less than 140/90 mm Hg. Serum total adiponectin and HMW adiponectin were measured at study entry (baseline), the 3-month treatment time point, and the end of the 6-month period. Non-HMW adiponectin (ie, medium- and low-molecular weight adiponectin) was calculated as total adiponectin − HMW adiponectin. Diagnosis of MS was done by current standard criteria. In hypertensive patients without MS (n = 21), the serum total adiponectin increased from 9.8 ± 5.4 μg/mL at baseline to 11.1 ± 6.2 μg/mL at 6 months (P < .01). Furthermore, the serum total adiponectin was significantly higher at 6 months than at 3 months (P < .01). Serum HMW adiponectin also increased from 5.7 ± 3.9 μg/mL at baseline to 6.6 ± 4.4 μg/mL at 6 months (P < .01). In hypertensive patients with MS, the serum total adiponectin increased from 6.0 ± 2.7 μg/mL at baseline to 6.7 ± 3.3 μg/mL at 3 months and to 7.0 ± 3.1 μg/mL at 6 months (P < .01 for both). Furthermore, the serum HMW adiponectin concentration was significantly higher at 6 months than at 3 months (P < .001). However, the serum non-HMW adiponectin concentration did not change during treatment in either group. In conclusion, serum total and HMW adiponectin concentrations increase after 6 months of losartan treatment in hypertensive patients, irrespective of the presence or absence of MS.     

Hormone replacement therapy causes a decrease in hepatocyte growth factor in hypertensive women

OBJECTIVE: Serum hepatocyte growth factor (HGF) is associated with blood pressure. We investigated whether the serum HGF level differs between hypertensive and normotensive postmenopausal women (PMW) and whether hormone replacement therapy (HRT) alters the serum HGF level and blood pressure in hypertensive and normotensive PMW. DESIGN: Prospective observational study. METHODS: A total of 33 PMW with mild to moderate essential hypertension controlled by antihypertensive treatment (mean age, 57 +/- 6 years) and 23 normotensive PMW (mean age, 57 +/- 7 years) received continuous HRT (0.625 mg of conjugated equine estrogen combined with 2.5 mg of medroxyprogesterone acetate) once a day orally for 12 months, and we measured serum HGF levels and blood pressure before and 12 months after the start of HRT. RESULTS: The baseline serum HGF level was significantly higher in hypertensive PMW than in normotensive PMW. HRT significantly decreased the serum HGF level in hypertensive subjects, from 2.85 +/- 0.64 pmol/l to 2.49 +/- 0.65 pmol/l (P < 0.001), but not in normotensive subjects. HRT did not change blood pressure in either group. CONCLUSIONS: Serum HGF level before the start of HRT was higher in the hypertensive PMW than in the normotensive PMW. Furthermore, HRT decreases serum HGF without decreasing blood pressure in hypertensive PMW. The HRT-induced decrease in serum HGF was greater in hypertensive PMW than in normotensive PMW, and the decrease was independent of blood pressure changes.     

血清肝细胞生长因子与高血压患者合并急性冠脉综合征的相关性

目的 探讨肝细胞生长因子（HGF）在原发性高血压及急性冠脉综合征（ACS）患者血清中的表达水平及其临床意义.方法 采用双抗体夹心酶联免疫荧光吸附法（ELISE）测定25例单纯高血压患者、20例高血压合并不稳定型心绞痛（UA）患者、25例高血压合并急性心肌梗死（AMI）患者、25名健康者的HGF血清浓度.结果 单纯高血压组、高血压合并UA组和高血压合并AMI组血清HGF浓度较正常对照组明显高,差异有统计学意义（P＜0.01）;高血压合并UA组、高血压合并AMI组血清HGF浓度较单纯高血压组明显高,差异有统计学意义（P＜0.05）;高血压合并AMI组血清HGF浓度较高血压合并UA组明显高,差异有统计学意义（P＜0.05）.结论 高浓度的HGF与血管内皮损伤和修复以及不稳定的粥样斑块破裂有关.测定HGF浓度将成为早期诊断高血压及其分级的重要指标和早期筛查不稳定冠状动脉粥样硬化斑块的新手段.     

Hepatocyte growth factor (HGF) as a potential index of severity of hypertension.

Hepatocyte Growth Factor (HGF) is a mesenchyme-derived pleiotropic factor that regulates cell growth, cell motility, and morphogenesis of various cells, and is thus considered a humoral mediator of epithelial-mesenchymal interactions. We previously identified HGF as a novel member of the family of endothelium-specific growth factors. Moreover, the presence of a local HGF system (HGF and its specific receptor, c-met) has been demonstrated in vascular cells both in vitro and in vivo. HGF might contribute to the protection and/or repair of vascular endothelial cells injured by high blood pressure. If so, serum HGF level might be elevated in response to endothelial cell damage. To test this hypothesis, we measured serum levels of HGF in hypertensive and normotensive patients. Serum HGF concentration in hypertensive patients without any complications was significantly higher than that in normal subjects. Interestingly, serum HGF concentration in hypertensive patients with complications was significantly higher than that in either hypertensive patients without complications or normotensive subjects. Of importance, hypertensive patients treated with antihypertensive drugs showed the same level of serum HGF concentration as normotensive subjects. In contrast, serum HGF concentration in diabetic patients without hypertension was significantly lower than that in normal subjects, whereas serum HGF concentration in diabetic patients with hypertension was significantly higher than that in normal subjects. Moreover, serum HGF concentration in diabetic patients with hypertensive complications was even higher than that in diabetics without complications. This review discusses the possibility that HGF may be considered as a new index of the severity of hypertension.