肝硬变患者血浆内皮素和心钠素的变化

探讨内皮素(ET)与肝硬变水纳潴溜的关系。方法:应用放免法测定了血浆内皮素(ET)和心纳素(ANP)的含量。结果:①68例肝硬变患者血浆ET水平与正常人相比明显低下(P<0.01),按Child-Pugh分级,可见ET在伴腹水的患者下降明显(B、C级);②ET与门静脉直径呈负相关(r=-0.769,P<0.05),门静脉直径>1.6cm者与直径<1.6cm者相比,ET含量差异亦有显著性意义(P<0.01);③肝硬变患者ANP值明显高于正常对照组(P<0.01),且ANP与ET水平呈负相关(r=-0.786,P<0.01)。结论:ET水平与肝硬变严重程度密切相关,ET可能在腹水形成机制中发挥了重要作     

慢性肝病患者血浆内皮素、内毒素及肿瘤坏死因子水平的研究

目的探讨慢性肝炎、肝硬变患者血浆内皮素（ET），内毒素（ETM）及肿瘤坏死因子（TNF-α）的变化及致病机制，以及它们之间相互关系．方法正常人20例，慢性肝炎20例，肝硬变48例．采用特异性放免分析法测定血浆ET和TNF－α含量．用基质显色法鲎试验定量检测血浆ETM含量．结果①肝硬变组血浆ET，ETM，TNF－α水平明显高于正常人和慢性肝炎组（P＜0．01）．②肝硬变合并肝肾综合征和食管静脉曲张者血浆ET水平高于腹水和不伴腹水者（P＜0．01）．③ET水平的增高与ETM，TNF－α水平呈显著相关性（r=0．614，P＜0．01）．结论ET参与肝硬变发病，与门脉高压形成密切相关，ET的生物学效应与ETM，TNF－α密切相关．     

肝硬变患者的血浆内皮素水平检测及其临床意义

内皮素(ET)是一种血管活性肽,它广泛分布于肝脏和门脉系统,对肝脏有重要的生物学效应。我们对50例肝硬变患者进行ET检测,探讨ET在肝硬变腹水产生中的作用,以及ET手术前后的动态变化和可能发生的病理影响。临床资料:选择肝硬变患者50例,男42例,女8例;年龄26～73岁,平均47.8岁。均为失代偿期,合并门静脉高压、食管胃静脉曲张,无心脏病、高血压及肾功不全,近期无上消化道出血、感染等。21例合并腹水(大量10例,中等量6例,少量5例),其中8例内科治疗后腹水消退。肝功Child分级,A级16例,B级21例,C级13例。其中31例行脾切除 门静脉奇静脉断流术…     

洛沙坦对肝硬变患者血浆一氧化与内皮素的影响

目的探讨肝硬变患者血浆一氧化氮(NO)、内皮素(ET)水平的变化及洛沙坦对这些物质的影响.方法选择20例正常人为对照组,46例肝硬变患者,男32例,女14例,肝功能A级12例,B级15例,C级19例.用化学比色法和放射免疫法分别测定其血浆硝酸盐/亚硝酸盐及内皮素水平.内镜下测定食管静脉曲张程度.32例患者用洛沙坦治疗4wk,并进行治疗前后的对比分析.结果肝硬变患者血浆NO与ET水平显著高于正常人(56.18±18.80vs18.25±3.10;89.98±25.38vs49.62±9.07,t值分别为8.92和6.89,P<0.001),且两者水平变化呈正相关(r=0.41,0.005<P<0.01);随着肝硬变程度的加重,血浆中NO,ET浓度逐渐升高,C级患者血浆中NO浓度与A级比较有显著差异(P<0.01),ET浓度在三组中任意两组比较均有差异(P<0.001);治疗组治疗后各级NO与ET水平均明显下降,其中A,B级患者NO,ET浓度下降较C级明显,但仍高于正常对照组;血浆NO,ET浓度变化与食管静脉曲张程度相平行.结论洛沙坦能显著降低肝硬变患者血浆NO与ET水平,降低门脉压力,减少并发症.     

肾素、血管紧张素Ⅱ及抗利尿激素与肝硬化腹水形成的关系

目的肾素-血管紧张素-醛固酮系统（RAAS）、抗利尿激素（ADH）与腹水的形成有着密切的关系，本研究旨在通过观察肝硬化患者血浆肾素活性（PRA）、血管紧张素Ⅱ（AngⅡ）以及ADH水平，探讨PRA、AngⅡ及ADH与肝硬化患者腹水形成的关系。方法选择47例肝硬化患者，其中Child—Pugh分级A级13例，B级19例，c级15例，肝硬化无腹水13例，腹水伴肝肾综合征（hepatorenal syndrome，HRS）8例，腹水无HRS26例，应用放射免疫方法分别检测其血浆PRA、AngⅡ及ADH表达水平进行检测，并以30例健康人为对照组进行比较。结果（肝功能）Child—PughB级及C级患者PRAAngⅡ及ADH水平均明显高于对照组与A级组，肝硬化患者在未合并腹水时PRA、AngⅡ及ADH水平与对照组比较无显著差异，在出现腹水后，与对照组比较差异有显著意义（P〈0．01）。腹水伴HRS组与腹水无HRS组比较，有显著差异（P〈0．05）。结论肝硬化患者血浆PRA、AngⅡ及ADH与肝硬化腹水的形成密切相关。     

测定腹水氨浓度鉴别肝细胞癌的门脉栓塞

作者研究36例有腹水的肝病患者,其中肝硬变18例,肝细胞癌18例,36例均检查了腹水和血氨浓度。结果 18例肝硬变者腹水氨浓度高于血氨。18例肝细胞癌中9例门脉主干有肿瘤栓塞,该9例腹水氨浓度低于血氨,与肝硬变患者不同。门脉主干无肿瘤栓塞的9例中8例腹水氨浓度高于血氨,与肝硬变时相同,另1例腹水氨浓度低于血氨,该例黄疽显著,     

肝硬变腹水并低钠血症研究概况

低钠血症(血清钠离子<130mmol/L)是最常见的电解质紊乱。肝硬变腹水患者低钠血症的发生率为57％,重度低钠血症可引起持久性的严重中枢神经系统损害,病死率高达50％。对这方面的研究进展扼要介绍如下: 1.低钠血症脑病的发病机理在肝硬变腹水合并低钠血症的患者中,低钠血症对中枢神经的影响,比其对心血管系统、肌肉骨骼系统及肾脏的影响更大,而它对中枢神经系统的影响除了已知的通过渗透压感受器细胞刺激、控制ADH(抗利尿激素)的释放,进而控制血浆渗透压的变化外,近年来发现低钠血症所致脑病的主要原因     

肝硬变血清甲状旁腺激素与降钙素水平变化研究

目的探讨肝硬变患者血清甲状旁腺激素(PTH)与降钙素(CT)水平的变化及其与钙、磷代谢紊乱的关系,方法收集经临床诊断的肝硬变患者45例,肝炎后肝硬变43例,酒精性肝硬变2例,合并肝癌者2例.Child-Pugh肝功能分级B级17例,C级28例.对照组为体检健康者21例.晨起空腹经肘静脉取血3mL,用放免法检测PTH及CT,同时取血检测肝功能、白球蛋白、碱性磷酸酶、钙、磷、肌酐及尿素氮等.结果肝硬变组血清PTH和CT水平明显升高,与对照组比较有显著差异(P<0.01),肝功能C级较B级升高更为显著(P＜0.05).低血钙15例(占33.3%),高血磷3例.结论肝硬变肝功能受损,使PTH和CT的代谢、降解发生障碍,使之水平升高,影响肝硬变患者的钙磷代谢,再加上肝硬变患者的消化、吸收不良等因素,而引发肝性骨营养不良,临床上应予以重视,及时纠正和改善,以提高肝硬变患者的生活质量.     

血浆内源性阿片肽与实验性肝硬变及腹水形成的作用

目的探讨血浆内源性阿片肽(Eop)在实验性肝硬变及腹水形成过程中的变化的意义.方法应用放射免疫法测定正常对照组及CCl4诱发大鼠肝硬变(n=37)及形成腹水(n=17)过程中血浆3种Eop的含量变化.结果肝硬变腹水组及肝硬变组血浆亮氨酸脑啡肽(L-ENK)含量均显著高于正常对照组(P均＜0.01),且都与血清清蛋白浓度呈显著负相关(r=-0.69,P＜0.01; r=-0.56,P＜0.01);与凝血酶原时间(PT)呈显著正相关(r=0.68,P＜0.01; r=0.69,P＜0.01). 同样两肝硬变组血浆强啡肽(DynA1-13)含量均显著高于正常对照组(P均＜0.01). 且与血清清蛋白浓度呈显著负相关(r=-0.64,P＜0.01; r=-0.59,P＜0.01),与PT呈显著正相关(r=0.65,P＜0.01; r=0.67,P＜0.01). 但两肝硬变组血浆L-ENK,DynA1-13与血ALT不相关. β-内啡肽(β-EP)的血浆含量在两肝硬变组及正常对照组中无显著差异.结论肝脏灭活功能受损是血浆小分子阿片肽(L-ENK与DynA1-13)含量升高的重要原因,后者又是实验性肝硬变腹水形成的主要原因之一. 而在β-EP体内灭活过程中,肝脏不起主要作用.     

门静脉高压症脾切除术后患者血浆内皮素变化与门静脉血栓形成的关系

为探讨门静脉高压症患者脾切除术后血浆内皮素 (ET)水平变化及其临床意义 ,采用放免法测定了30例肝硬变门静脉高压症行脾切除术患者 (观察组 )术前及术后 1周血浆 ET水平 ,并设对照组比较。结果显示 ,观察组术前血浆 ET水平 (6 7.2 4± 2 4 .6 3pg/ml)明显高于对照组 (33.2 1± 11.0 5 pg/ml) ,P<0 .0 0 1;术后 1周明显下降 (37.2 4± 14 .4 7pg/ml) ,P<0 .0 0 1,与对照组 (32 .4 8± 10 .6 2 pg/m l)比较无显著差异 ,P>0 .0 5。脾切除术后门静脉血栓形成者 ET水平 (5 7.90± 2 1.70 pg/m l)明显高于非血栓形成者 (33.15± 8.2 9pg/ml) ,P<0 .0 0 1。认为ET在肝硬变、门静脉高压症发生中起重要作用 ,ET增高与门静脉血栓形成有关。脾切除术后血浆 ET明显下降 ,对改善肝脏功能、降低门静脉压力具有重要意义     

肝硬化患者血浆降钙素基因相关肽及内皮素-1水平的变化

目的 探讨肝硬化患者血浆降钙素基因相关肽（ＣＧＲＰ）及内皮素－１（ＥＴ－１）水平的变化,了解此二者之间及它们与肝硬化门脉高压形成及局长和肝功能损伤的关系。方法 用放免法检测２４例正常人和６１例肝硬化患者血浆ＣＧＲＰ和ＥＴ－１水平。结果 肝硬化组血浆ＣＧＲＰ及ＥＴ－１水平显著高于对照组,且在肝功能分级中,呈现ＣｈｉｌｄＣ〉Ｃｈｉｌｄ Ｂ〉ＣｈｉｌｄＡ的规律。组间分析表明肝硬化患者食管静脉曲张伴大中量     

不同临床类型慢性肝病患者血浆内皮素水平研究

目的探讨内皮素(endothelin,ET)与不同临床类型慢性肝病的关系。方法用放射免疫分析法测定62例慢性肝病组(包括慢性肝炎、肝硬化代偿期、肝硬化失代偿期组)患者血浆ET浓度,并进行横向比较。结果慢性肝病组ET水平较正常降低,差异有统计学意义(P<0.01),而慢性肝炎、肝硬化代偿期、肝硬化失代偿期ET水平比较差异无统计学意义(P>0.05)。结论(1)慢性肝病患者血浆ET水平显著降低;(2)血浆ET水平在慢性肝炎、肝硬化代偿期、肝硬化失代偿期患者之间差异无统计学意义。     

高血压病患者血浆内皮素和P物质的相关性研究

本文采用放射免疫分析法，对５４例高血压病（ＥＨ）患者浆内皮素（ＥＴ）、Ｐ物质（ＳＰ）的浓度进行检测。结果表明，治疗前ＥＨ组血浆ＳＰ较对照组明显降低（Ｐ＜０．０１），ＥＴ明显升高（Ｐ＜０．０１），血浆ＥＴ与ＳＰ之间呈显著负相关（ｒ＝－０．３５０，Ｐ＜０．０１）。用比索洛尔治疗１４天后，血浆ＳＰ明显升高，ＥＴ明显降低（Ｐ＜０．０１）．以上结果提示：血浆ＥＴ、ＳＰ可能参与高血压的发生机制，血浆ＥＴ、ＳＰ水平的失衡在高血压的发病中可能起重要作用。     

病毒性肝炎患者血浆一氧化氮和内皮素水平及意义

各型病毒性肝炎及活动性肝硬化患者共２１３例,采用镉柱还原法及重氮化法检测ＮＯ＾－２／ＮＯ＾－３水平,放免法检测了ＥＴ－１水平。急性肝为,慢性活动型肝炎,肝炎肝硬化等各型肝病患者血清ＮＯ＾－２／ＮＯ＾－３及ＥＴ－１水平均有不同程度的升高,肝炎急性期ＮＯ就有明显升高,慢性肝病ＮＯ与ＥＴ随病情进展水平升高,二者水平良好的相关性。     

Endothelin-1 derived from spleen-activated Rho-kinase pathway in rats with secondary biliary cirrhosis

Aim: Splenectomy or partial splenic embolism has been reported to improve liver function in patients with hypersplenism and liver dysfunction. The aim of this study was to investigate the mechanism of improvement after splenectomy. Methods: Liver cirrhosis was induced by bile duct ligation (BDL). Rats underwent sham operation, splenectomy (Sp group), BDL, or BDL plus splenectomy (BDL + Sp group), and were subjected to experiments at 2 weeks after the operation. Portal venous pressure (PVP) and hepatic tissue blood flow (HTBF) were measured in each group. The plasma concentration of endothelin‐1 (ET‐1) and endothelial nitric oxide synthase (eNOS), RhoA and Rho‐kinase expressions were studied. Results: There were significant differences in PVP (17.9 ± 0.91 vs 23.3 ± 3.91 cmH₂O; P < 0.01) and HTBF (16.6 ± 1.72 vs 13.3 ± 1.82 mL/min; P < 0.01) between the BDL + Sp and BDL groups. In the liver of BDL rats, eNOS phosphorylation and NOx levels were decreased, accompanied by RhoA activation compared with the BDL + Sp group. Splenectomy decreased serum ET‐1 levels, RhoA activation and consequently increased eNOS phosphorylation. Conclusion: ET‐1 derived from the spleen might increase intrahepatic resistance by downregulating Rho signaling in liver cirrhosis. Splenectomy for splenomegaly in liver cirrhosis might partially improve liver function by enhancing intrahepatic microcirculation.     

肝硬化患者肾血流及内皮素变化的临床研究

目的 研究肝硬化患者肾脏血液动力学的变化。 方法 对49例肝硬化患者,采用彩色多普勒超声测定肾叶间动脉及弓形动脉搏动指数(PI)、阻力指数(RI)、收缩期最高峰值(PS)、舒张期最低峰值(PD)及收缩期最高峰值/舒张期最低峰值(PS/PD)等指数,并同时监测患者的血内皮素情况。 结果 PI和RI随肝功能损伤加重而增高,尤以RI为著。肝功能Child分级A、B、C,RI值分别为0.60±0.09、0.66±0.06、0.72±0.07,F=10.005,P<0.01;随腹水量的增加,PI、RI等亦有明显增高:少量、中—大量、顽固性腹水组PI分别为1.14±0.20、1.31±0.29、1.42±0.36,F=28.747,P<0.05。RI分别为0.61±0.09、0.68±0.07、0.77±0.05,F=17.250,P<0.01。肝硬化患者血内皮素值增高为(1.26±0.27)ng/L,且与PI及RI增高呈正相关(相关系数分别为0.556、0.576)。 结论 肝硬化患者肾血流PI和RI的变化与肝功能及腹水的加重有密切相关。内皮素可能是参与肝硬化患者肾血管收缩的重要活性因子。     

Role of antidiuretic hormone in impaired water excretion of patients with congestive heart failure

Plasma antidiuretic hormone (ADH), PRA, plasma osmolality, and the parameters of renal water excretion were measured after overnight dehydration and for 5 h after an oral load in 14 patients with congestive heart failure (CHF) treated with diuretics (group 1), 8 hypertensive patients without CHF also treated with diuretics (group 2), and 11 patients with coronary artery disease but without CHF who were not treated with diuretics (group 3). Under basal conditions, mean plasma osmolality was lower in group 1 than in group 3, but was not different in groups 1 and 2. Mean plasma ADH was higher in group 1 than in group 2 or 3. In response to the water load, plasma osmolality and plasma ADH levels decreased in the 3 groups. ADH levels remained significantly greater in group 1 than in groups 2 and 3 from 2-4 h after the water load despite more marked hypoosmolality in group 1 compared with that in either of the 2 control groups. Plasma ADH was significantly correlated with plasma osmolality only in the 2 control groups. Mean PRA was greater in patients with CHF and patients without CHF treated with diuretics than in untreated patients. Cumulative water excretion was lower in patients with CHF than in patients in the 2 control groups from 2-5 h after the water load. At 5 h, the mean percentage excretion of the ingested loads was 56.8%, 90.7%, and 91.2% in the patients of groups 1, 2, and 3 respectively. Free water clearance was lower and minimal urinary osmolality was greater in the patients with CHF than in those in the 2 control groups. Two patients with CHF, who excreted more than 75% of the water load, also had low plasma basal ADH levels. These data show that patients with CHF have an inappropriate response of plasma ADH to a marked fall in plasma osmolality. This disorder is not due to the diuretic therapy, since hypertensive patients treated with diuretics behaved similarly to untreated patients without CHF. The reasons for this inappropriate response of plasma ADH during a water load in patients with CHF are probably multifactorial.     

Increased urinary endothelin excretion in patients with liver cirrhosis

The urinary endothelin level in patients with chronic liver disease was determined in order to explore its possible involvement in renal function. The plasma endothelin level was significantly higher in patients with liver cirrhosis (LC) than in those with chronic hepatitis (CH) or in control patients (C). Similarly, urinary endothelin excretion in LC was significantly increased, compared with CH and C. Urinary endothelin demonstrated a significant positive correlation with creatinine clearance. The ratio of endothelin clearance/creatinine clearance did not differ statistically among the three groups. Urinary sodium excretion in LC was positively correlated with plasma endothelin, but not with urinary endothelin. Urinary endothelin excretion demonstrated a significant negative correlation with urinary kallikrein in LC. The present data suggest that increased urinary endothelin excretion in cirrhotic patients primarily depends upon elevated plasma levels of endothelin, but not renal production. Also, a possible link between endothelin and the kallikrein-kinin system in liver cirrhosis is indicated.     

肝硬化患者血浆ET-1、NO和黏附分子的水平变化及临床意义

目的观察肝硬化患者血浆中内皮素(ET-1)、一氧化氮(NO)和可溶性细胞间黏附分子-1(sICAM-1)、可溶性血管细胞黏附分子-1(sVCAM-1)的水平变化及其与肝功能的关系,探讨其临床意义。方法采用放射免疫、分光光度及单克隆抗体法,分别检测肝硬化患者血浆中的ET-1、NO和sICAM-1、sVCAM-1水平并与正常对照组进行对比分析。结果肝硬化组(观察组)血浆ET-1、NO和sI-CAM-1、sVCAM均明显高于对照组。肝功能Child-Pugh分级A级与对照组之间无明显差异(P>0.05),B、C级与对照组之间差异显著(P<0.01),A、B、C级之间的差异非常显著(P<0.01)。结论肝硬化患者血浆ET-1、NO和sICAM-1、sVCAM-1水平均升高,并与肝细胞损伤、肝功能障碍呈正相关,提示血浆ET-1、NO和sICAM-1、sVCAM-1水平监测可作为临床观察肝硬化患者病变活动的重要免疫学指标,对肝硬化的早期诊断和Child-Pugh分级具有一定的参考和补充价值。     

肝硬化亚临床肾病的诊断方法及肾病形成机制的探讨

我们用放射免疫分析方法检测了肝硬化患者尿中3种微量蛋白,同时测定了血清部分免疫球蛋白和补体。结果,43例肝硬化一般肾功能正常患者尿白蛋白明显增高者29例(67％),尿IgG增高者24例(55％),THP增高者18例(42％),与正常对照组比差异具显著性。血清IgA显著升高,且与尿白蛋白增高相平行,但不同肝功能分级间无明显变化。因此,我们认为血清IgA升高与肝硬化肾病形成有关,尿微量蛋白测定可作为肝硬化亚临床肾病的诊断方法。