软肝方合麝黄膏敷脐及腹水超滤浓缩回输治疗顽固性肝硬化腹水的临床研究

目的：观察软肝方合麝黄膏敷脐及腹水超滤浓缩回输治疗顽固性肝硬化腹水的临床疗效。方法：120例顽固性肝硬化腹水住院患者,随机分为治疗组和对照组,每组各60例。对照组患者在西药常规治疗的基础上加用腹水超滤浓缩回输,频率为两周1次,疗程为1个月;治疗组患者在对照组治疗的基础上加用麝黄膏外敷脐部,1贴/次,1次/d,疗程为1个月,同时加服软肝中药颗粒,1包/次,2次/d,疗程为3个月。观察患者腹水消退、肝功能、凝血功能、血浆内毒素、NO（一氧化氮）和ET（内皮素）的变化。结果：治疗组患者腹水消退在治疗3个月和6个月的总有效率分别为70%、73.3%,明显优于对照组的20%和15%（P〈0.01）;两组患者治疗后1、3、6个月ALT（丙氨酸转氨酶）、TB il（总胆红素）均较治疗前明显下降（P〈0.01）,治疗组在治疗后3个月、6个月时ALT、TB il下降更显著,与对照组同期比较,差异有显著性意义（P〈0.05或P〈0.01）;在PT（凝血酶原时间）的改善上,两组在治疗后3个月、6个月时均较治疗前显著下降,差异有显著性意义（P〈0.05）,但两组之间差异无显著性意义（P〉0.05）。两组在治疗后1个月均可明显降低血浆内毒素和NO、ET含量（P〈0.05或P〈0.01）;在治疗后3个月、6个月时对照组又恢复至治疗前水平;而治疗组患者血浆内毒素、NO、ET含量较治疗前明显下降,与治疗前和对照组同期比较,差异均有显著性意义（P〈0.05或P〈0.01）。结论：软肝方配合麝黄膏敷脐及腹水超滤浓缩回输治疗肝硬化顽固性腹水能有效地消退腹水,减轻内毒素血症和血管活性物质的产生,防止腹水的短期复发。     

中药联合腹水超滤浓缩回输法治疗肝硬化顽固性腹水的临床研究

目的：观察中药联合腹水超滤浓缩回输法治疗肝硬化顽固性腹水的疗效。方法：选择肝硬化顽固性腹水住院患者62例，随机分为两组，治疗组32例，采用中药＋腹水超滤浓缩回输＋基础治疗；对照组30-ff0，采用腹水超滤浓缩回输＋基础治疗。疗程均为1个月．腹水超滤浓缩回输的频率为2周1次，1次超滤的腹水为3000ml-8000ml，观察治疗前后患者的体重、腹围、24小时尿量、血浆白蛋白、腹水白蛋白、门脉主干的血流动力学变化及患者血浆和腹水中内毒素水平的变化。结果：两组患者的临床症状均得到较好改善，患者体重及腹围显著下降，24小时尿量增加，血浆及腹水中蛋白量增加，治疗组患者门静脉、脾静脉内径及血流量、血浆中内毒素水平较治疗前显著下降，对照组患者则无明显改善，两组比较差异有显著性意义（P〈0．05）；治疗组患者腹水Ⅰ级消退者18例，占56．3％，对照组只有4例，占13.3％，两组比较差异有显著性意义（P〈0．05）。结论：中药联合腹水超滤浓缩回输治疗肝硬化顽固性腹水有较好疗效，其作用机制可能与改善患者血浆内毒素水平有关。     

Effect of somatostatin versus octreotide on portal haemodynamics in patients with cirrhosis and portal hypertension

OBJECTIVES: Elevated portal inflow is part of the pathogenesis of portal hypertension in patients with cirrhosis. Vasoactive substances appear to play a primary role in the regulation of portal flow. The aim of this study was to investigate the effects of somatostatin and octreotide on portal pressure and plasma levels of insulin-like growth factor (IGF-1), nitric oxide (NO), endothelin-1 (ET-1) and glucagon (GLU). METHODS: Portal pressures of 14 cirrhotic patients with portal hypertension who underwent transjugular intrahepatic portosystemic shunt (TIPS) were directly measured via a catheter placed in the portal vein. Portal pressure and IGF-1, NO, ET-1 and GLU plasma levels were determined at baseline, and at 8 h and 24 h after administration of somatostatin or octreotide via portal vein catheter in a randomized, double-blind, cross-over design. RESULTS: The average decrease in portal pressure after intravenous infusion of somatostatin and octreotide was 9.4 +/- 1.0 cmH2O and 5.0 +/- 1.0 cmH2O, respectively (P < 0.01). Plasma levels of GLU and IGF-1 decreased significantly 8 and 24 h after somatostatin and octreotide infusion (P < 0.05). However, there were no significant decreases in plasma NO or ET-1 levels. There was a significant difference between somatostatin and octreotide groups (P < 0.01). CONCLUSION: Both somatostatin and octreotide can significantly reduce portal pressure, although somatostatin is more potent than octreotide. The underlying mechanisms may involve inhibition of the secretion of GLU, IGF-1 and other hormones as well as a decrease in hepatic metabolism and portal inflow leading to a reduction in portal pressure.     

Role of endotoxaemia in hyperdynamic circulation in rats with extrahepatic or intrahepatic portal hypertension

This study investigated the role of endotoxaemia in the development of hyperdynamic circulation observed in rats with extrahepatic (high collateralization) or intrahepatic (low collateralization) portal hypertension. Compared with sham-operated rats, decreased mean arterial pressure and systemic vascular resistance were detected on days 1, 4 and 14 following partial portal vein ligation. By day 1, the cardiac index of portal vein-ligated rats was similar to that of sham-operated rats and progressively increased, thereafter, reaching statistically higher values on days 4 and 14. No differences in plasma endotoxin levels were found between portal vein-ligated and sham-operated rats throughout the observation period. Both carbon tetrachloride-induced cirrhotic rats with and without ascites had a higher cardiac index and lower systemic vascular resistance than those of control rats, and cirrhotic rats with ascites had the lowest systemic vascular resistance. Plasma endotoxin levels were higher in cirrhotic rats with ascites (8.6±2.0 pg/mL; P < 0.01) than those of control rats (2.2±0.3 pg/mL) and cirrhotic rats without ascites (2.4±0.6 pg/mL). These results suggest that factors other than endotoxaemia play a role in the development of hyperdynamic circulation observed in rats with extrahepatic portal hypertension and cirrhotic rats without ascites, but that endotoxaemia may contribute to the maintenance of hyperdynamic circulation found in cirrhotic rats with ascites. The severity of liver disease may be a more important factor than the presence of portosystemic shunting for the development of endotoxaemia in portal hypertensive states.     

特利加压素联合前列地尔辅助腹水超滤浓缩回输治疗肝硬化并发难治性腹水患者疗效分析*

目的 探讨应用特利加压素联合前列地尔辅助腹水超滤浓缩回输治疗肝硬化并发难治性腹水患者的临床效果。方法 2017年3月～2018年6月我院感染病科住院治疗的104例肝硬化并发难治性腹水患者被随机分为腹水回输治疗组52例和综合治疗组52例,分别给予腹水超滤浓缩回输腹腔治疗,综合治疗组则在此基础上加用前列地尔和特利加压素治疗。观察6个月。结果 治疗后一周,综合治疗组门静脉血流速度(Vpv)和脾静脉血流速度(Vsv)分别为(25.6±1.5)cm/s和(27.3±2.7)cm/s,显著快于腹水回输组【分别为(21.4±1.3)cm/s和(25.4±2.1)cm/s, P<0.05】;治疗后,综合治疗组血清一氧化氮、内皮素-1和内毒素水平分别为(13.4±2.1)μmol/L、(53.2±10.3)pg/mL和(31.4±13.2)pg/mL,与腹水回输组【分别为(16.2±2.3)μmol/L、(68.3±12.6)pg/mL和(49.5±14.1)pg/mL,P<0.05】比,差异显著;治疗后,综合治疗组腹围、腹水量和24 h尿量分别为(98.6±7.2)cm、(35.2±9.3)mm和(1531.4±234.2)mL,与腹水回输组【分别为(102.7±6.4)cm、(48.3±11.5)mm和(1249.5±215.1)mL, P<0.05】比,差异显著;治疗后6个月,综合治疗组腹水消退35例(67.3%),显著高于腹水浓缩回输组的14例(26.9%,P<0.05)。结论 应用特利加压素联合前列地尔辅助腹水超滤浓缩回输腹腔治疗肝硬化并发难治性腹水患者具有较好的临床治疗效果,可显著改善患者血液微循环和肝肾功能,有助于促进腹水消退,维持疗效。     

肝硬化患者血浆内皮素和胰高血糖素水平的变化及其临床意义

目的 研究肝硬化时血浆内皮素-1(ET-1)和胰高血糖素(GLU)水平的改变及其与肝功能损害和门脉高压形成的关系。方法 采用放射免疫分析法测定40例肝硬化患者和18例对照组空腹血浆ET-1和GLU水平。用彩色多普勒超声测定门静脉及脾静脉的直径、流速和流量。结果 肝硬化患者血浆ET-1和GLU水平显著高于对照组。按肝功能Child-Pugh分级将肝硬化患者分为A、B、C三组，各组血浆ET-1和GLU水平依次升高。合并腹水的肝硬化患者血浆ET-1和GLU水平显著高于未合并腹水者。血浆ET-1和GLU水平与门静脉和脾静脉的直径以及脾静脉的流量呈显著正相关。结论 肝硬化患者血浆ET-1及GIU水平升高反映了肝功能损害的严重程度，同时在门静脉高压的形成和发展过程中起着重要的作用。     

1型肝肾综合征患者内毒素和内皮素1水平分析

目的分析肝硬化腹水伴1型肝肾综合征(HRS)患者的临床资料、实验室指标、感染发生率、血清降钙素原(PCT)和内皮素1(ET-1)水平,探讨内毒素和ET-1在HRS发生中的作用。方法纳入本院2009年1月至2012年10月住院的肝硬化腹水伴1型HRS患者56例(HRS组)及肝硬化伴腹水且肾功能正常患者60例(非HRS组),收集2组患者的一般资料、肝硬化病因、感染发生率及类型、Child-Pugh分级、全身炎症反应综合征(SIRS)评分及平均动脉压(MAP);同时采集2组患者血液,分析肝肾功能、电解质、PCT、ET-1水平。比较2组患者的临床资料和检测指标。计数资料采用χ2检验,正态分布计量资料组间比较采用成组t检验,非正态分布计量资料组间比较采用Wilcoxon秩和检验。结果 HRS组感染发生率为75.0%,显著高于非HRS组的28.4%(χ2=11.91,P0.05)。HRS组PCT、ET-1和SIRS分别为8.72(3.14,31.68)ng/L、(13.04±2.82)pg/ml和2.1±1.1,高于非HRS组的0.11(0.04,0.45)ng/L、(5.76±1.68)pg/ml和0.6±0.6(P0.05)。实验室指标中,HRS组血清尿素、肌酐、半胱氨酸蛋白酶抑制剂及钾水平高于非HRS组,差异有统计学意义(P0.05);而HRS组的Na、Cl水平低于非HRS组,差异有统计学意义(P0.05),两组间ALT、AST差异无统计学意义(P0.05)。结论内毒素诱导ET-1表达增加,ET-1强烈收缩肾血管引发肾灌注不足,导致1型HRS的产生。内毒素和ET-1与1型HRS发生关系密切。     

Ultrasonic diagnosis and vasoactive substances examination in patients with cirrhosis

Objective:To investigate hemodynamic change of patients with cirrhosis by using Color Doppler ultrasound technique and to explore the significance of change in the content of vasoactive substances-plasma endothelin-1(ET-1)and calcitonin gene-related peptide(CGRP).Methods:A total of 178 cases with cirrhosis were regarded as study groups,and were divided into three degrees:A,B and C according to child-pugh and meanwhile 60 cases were regarded as normal control group.Portal vein and splenic vein of patients were explored by adopting Color Doppler ultrasound technique,related indexes were recorded and the blood flow as well as their ration in the two groups was calculated.Radio immunoassay was adopted to detect the content of plasma ET-1 and CGRP in both study group and contrast group.Results:Compared with the healthy cases in the contrast group,there was abnormal hemodynamics in the system of portal vein of patients with cirrhosis and the content of plasma ET-1 and CGRP was increased obviously.In the Child-Pugh liver function grades,the content of ET-1 and CGRP was increased as the degree of cirrhosis became more and more serious.There was no significant difference in the comparison between those without ascites and those in contrast group(P0.05),the content of plasma ET-1and CGRP in patients without ascites was increased remarkably.Besides,there was positive correlation between the content of plasma ET-1 and CGRP and Dpv,Dsv and Qsv.Conclusion:Dotection of abnormal hemodynamics of portal vein and splenic vein by Color Doppler ultrasound technique can be one of the means for diagnosis of hypertension.Plasma ET-1 and CGRP of patients with cirrhosis reflect the serious degree of the damage in live function and play an important role in the formation and development of portal hypertension.     

Effects of tumor necrosis factor, endothelin and nitric oxide on hyperdynamic circulation of rats with acute and chronic portal hypertension

AIM:To evaluate the effect of tumor necrosis factor (TNF),endothelin (ET) and nitric oxide (NO) on hyperdynamic circulation (HC) of rats with acute and chronic portal hypertension (PHT).METHODS: Chronic portal hypertension was induced in Wistar rats by injection of carbon tetrachloride. After two weeks of cirrhosis formation, L-NMMA (25mg/kg) was injected into one group of cirrhotic rats via femoral vein and the experiment was begun immediately. Another group of cirrhotic rats was injected with anti-rat TNFα (300mg/kg) via abdominal cavity twice within 48h and the experiment was performed 24h after the second injection. The blood concentrations of TNFα, ET-1 and NO in portal vein and the nitric oxide synthase (NOS) activity in hepatic tissue were determined pre-and post-injection of anti-rat TNFα or LNMMA. Stroke volume (SV), cardiac output (CO), portal pressure (PP), superior mesenteric artery blood flow (SMA flow) and lilac artery blood flow (IAflow) were measured simultaneously. Acute portal hypertension was established in Wistar rats by partial portal-vein ligation (PVL). The parameters mentioned above were determined at 0.5h,24h, 48h, 72h and 120h after PVL. After the formation of stable PHT, the PVL rats were injected with anti-rat TNFα or L-NMMA according to different groups, the parameters mentioned above were also determined.RESULTS:In cirrhotic rats, the blood levels of TNFα, NO in portal vein and the liver NOS activity were significantly increased (P&lt;0.05) while the blood level of ET-1 was not statistically different (P&gt;0.05) from the control animals(477.67&#177;83.81pg/mL vs 48.87&#177;32.79pg/mL, 278.41&#177;20.11μmol/L vs 113.28&#177;14.51μmol/L, 1.81&#177;0.06μ/mg.prot vs 0.87&#177;0.03μ/mg.prot and 14.33&#177;4.42pg/mL vs8.72&#177;0.79pg/mL, respectively). After injection of anti-rat TNFα,the blood level of TNFα was lower than that in controls (15.17&#177;18.79pg/mL vs 48.87&#177;32.79pg/mL). The blood level of NO and the liver NOS activity were significantly decreased, but still higher than those of the controls. The blood level of ET-1 was not significantly changed. PP,SV,CO, SMAflow and IAflow were ameliorated. After injection of L-NMMA, the blood level of NO and the liver NOS activity were recovered to those of the controls. PP and CO were also recovered to those of the controls. SV, SMAflow and IAflow were ameliorated. In PVL rats, the blood levels of TNFα NO in portal vein and the liver NOS activity were gradually increased and reached the highest levels at 48h after PVL. The blood level of ET-1 among different staged animals was not significantly different from the control animals. PP among different staged animals (2.4&#177;0.18kPa at 0.5h, 1.56&#177;0.08kPa at 24h, 1.74&#177;0.1kPa at 48h,2.38&#177;0.05 kPa at 72h, 2.39&#177;0.16 kPa at 120h) was significantly higher than that in controls (0.9&#177;0.16kPa). After injection of anti-rat TNFα in 72h PVL rats, the blood level of TNFα was lower than that in controls (14&#177;14pg/mL vs 48.87&#177;32.79pg/mL). The blood level of NO and the liver NOS activity were significantly decreased, but still higher than those of the controls. The blood level of ET-1 was not significantly changed. PP was decreased from 2.38&#177;0.05kPa to 1.68&#177;0.12kPa, but significantly higher than that in controls. SV, CO, SMAflow and IAflow were ameliorated.After injection of L-NMMA in 72h PVL rats, the blood level of NO and the liver NOS activity were recovered to those of the controls. PP, SV, CO, SMAflow and IAflow were also recovered to those of the controls.CONCLUSION:NO plays a critical role in the development and maintenance of HC in acute PHT and is a key factor for maintenance of HC in chronic PHT. TNFα may not participate in the hemodynamic changes of HC directly, while play an indirect role by inducing the production of NO through activating NOS. No evidence that circulating ET-1 plays a role in both models of portal hypertension has been found.     

腹水的消长对于门静脉和脾静脉宽度的影响

对32例伴有张力型腹水的肝硬化患者,在腹水消失前后,用B超进行了门脾静脉内径及脾脏厚度的测定。结果表明:门静脉内径及脾脏厚度无明显变化(P>0.05),而脾静脉内径却在腹水消失后有增宽的趋势(P<0.05)。本文对形成上述现象的原因进行了探讨。     

麝黄膏脐敷治疗肝硬化难治性腹水临床研究

目的 :观察麝黄膏治疗肝硬化难治性腹水的疗效。方法 :选择肝硬化难治性腹水住院患者 ,治疗组 (32例 )采用基础治疗 +麝黄膏脐敷 ,对照组 (2 7例 )采用基础治疗 (包括保肝药物 ,利尿剂 ,白蛋白 ,抗生素等 )。观察治疗前后患者的体重、2 4 h尿量和尿电解质、肝功能以及血清一氧化氮 (NO)含量。彩色多普勒测量门脉血流量。结果 :治疗组总有效率为 84 .0 % ,对照组总有效率为 4 9.1%。治疗组治疗后体重、腹围明显下降、肝功能明显改善 ,2 4h的尿量增多。治疗组 NO含量、门脉血流量明显下降 (P <0 .0 5 ) ,而对照组无明显改善 (P >0 .0 5 )。结论 :麝黄膏脐敷对肝硬化难治性腹水有明显的治疗作用 ,比单纯基础治疗疗效高。     

Evaluation of portal circulation through the superior mesenteric vein with an enteric capsule of [123I]iodoamphetamine

We report a method by which the contribution of the superior mesenteric vein to the portal blood flow can be evaluated noninvasively. An enteric-coated capsule containing [¹²³I]iodoamphetamine is given by mouth 3 h before the examination. The data obtained are treated by computer to calculate the portal shunt index (SI) through the superior mesenteric vein. The SI was higher for more severe liver disorders, Increasing in the order of chronic persistent hepatitis, chronic aggressive hepatitis, and cirrhosis. The SI was higher in cirrhotic patients than in chronic hepatitis patients or healthy volunteers (both,P<0.001). The SI was higher in cirrhotic patients with esophageal varices than in such patients without varices (P<0.05). The SI was higher in cirrhotic patients with ascites than in such patients without ascites (P<0.001). The SI was higher in cirrhotic patients with encephalopathy than in those without encephalopathy (P < 0.01). Correlation was significant between the SI and classical indicators of functional reserve. This method is clinically useful.     

Hepatic dysfunction in patients with extrahepatic portal venous obstruction

Background: Extrahepatic portal venous obstruction (EHPVO) developing due to thrombotic occlusion of the portal vein in children is generally considered a benign disease. Whether hepatic dysfunction develops in these patients in the absence of a gastrointestinal bleed has not been well studied. Materials and methods: Forty‐three patients with EHPVO who had not bled in the last 3 months were studied. Patients were divided into those with (group I) or without ascites (group II). Matched cirrhotic patients with ascites (group III) served as controls. Clinical, biochemical, ultrasonographic, and histopathological evaluation was carried out. Portal biliopathy was assessed in five patients in group I and in 12 patients in group II by cholangiography. Results: Of 43 EHPVO patients, ascites was seen in nine (21%) patients (group I). Thirty‐four patients had no ascites (group II). Serum ALT (54±24 vs. 34±10 IU/l, P<0.01), albumin (3.2±0.3 vs. 3.7±0.4 g/dl, P<0.01), and prothrombin time difference (9.0±4.5 vs. 2.4±1.9 s, P<0.05) were deranged in patients in group I compared with group II. Patients in group I were 4 years older, and the duration of portal hypertension was longer than in group II (11.5 vs. 5.6 year, P<0.05). Portal biliopathy changes were significantly more severe in group I than in group II patients. Ascites was high gradient in all the patients in group I and the serum‐ascitic albumin gradient was comparable between groups I and III. None of the EHPVO patients, but four cirrhotic patients, developed spontaneous bacterial peritonitis during a follow‐up of 11±4 months. Conclusions: Hepatic dysfunction in the form of ascites and deranged liver functions is not uncommon in patients with EHPVO, more so in patients with prolonged portal hypertension. Based on our data it would be worthwhile to study whether prolonged portal vein thrombosis in EHPVO patients could lead to progressive liver disease.     

乙型肝炎肝硬化患者发生食管胃静脉曲张破裂出血的危险因素分析

目的探索乙型肝炎肝硬化患者发生食管胃静脉曲张破裂出血的危险因素。方法选取2014年10月—2016年6月因乙型肝炎肝硬化并发食管胃静脉曲张来我院进行治疗的患者165例,根据就诊当天是否发生破裂出血分为出血组和非出血组,分析该类患者破裂出血的危险因素。结果单因素分析结果显示:2组患者在年龄、性别和WBC计数方面的差异无统计学意义(P0.05),出血组患者HGB、PT明显高于非出血组,而PLT明显低于非出血组,差异有统计学意义(P0.05);出血组患者中肝功能Child-Pugh评分C级患者、重度食管胃静脉曲张患者及中重度腹水患者明显多于未出血组,2组患者在肝功能Child-Pugh评分、食管胃静脉曲张和腹水严重程度上的差异有统计学意义(P0.05)。多因素分析结果显示:肝功能Child-Pugh评分、PLT、腹水、门静脉内径和感染是发生破裂出血的危险因素,其中腹水严重程度是最主要的独立危险因素。结论肝功能Child-Pugh分级较低、PLT较低、腹水较严重、门静脉内径较大和出现感染是乙型肝炎肝硬化患者发生食管胃静脉曲张破裂出血的危险因素,临床上须尽早进行对症治疗,预防破裂出血的发生。     

大鼠实验性肝硬化门脉高压形成过程中血浆内皮素—1和一氧化氮的动态变化

目的 观察大鼠肝硬化门脉高压形成过程中外周血浆内皮素-1(ET-1)和一氧化氮(NO)的动态变化,以探讨两种物质在门脉高压高动力循环中的作用。方法 肝硬化门脉高压组大鼠模型用四氯化碳加乙醇制备,对照组只注射等量橄榄油。放免法检测血浆ET-1水平,硝酸还原酶法检测NO,观察两者在不同时期的变化。结果 模型制备过程中的第0、2和6周未见两组动物之间存在NO和ET-1水平的显著性差异,第10周时有ET-1水平的降低和NO水平的显著升高,同时有门脉压力的增高和体循环平均动脉压的降低。结论ET-1水平的降低和NO水平的增高是引起肝硬化门脉高压高动力循环产生的重要原因。     

Sodium handling in patients with well compensated cirrhosis is dependent on the severity of liver disease and portal pressure

BACKGROUND AND AIMS: To test the contribution of portal pressure gradient (PPG) and neurohumoral factors to sodium handling in cirrhotic patients without ascites, by comparing preascitic cirrhotic patients with patients with transjugular intrahepatic portosystemic stent shunt (TIPSS) and previous ascites. PATIENTS: Ten patients with TIPSS and 10 preascitic cirrhotic patients. METHODS: Changes in glomerular filtration, renal plasma flow, urinary sodium excretion (U(Na)V), and neurohumoral factors were measured before and for two hours after infusion of one litre of 0. 9% saline over one hour. RESULTS: Glomerular filtration rate and renal plasma flow were significantly higher in patients with TIPSS compared with preascitic cirrhotic patients. Following saline infusion both parameters increased significantly; this increase was significantly greater in patients with TIPSS. U(Na)V increased significantly in both groups following saline infusion. The increase in U(Na)V was significantly greater in the TIPSS group. Plasma renin activity and angiotensin II decreased significantly in both groups. Basal U(Na)V was independently correlated with angiotensin II concentration and PPG and the change in U(Na)V correlated with the PPG. CONCLUSIONS: Results suggest that patients with advanced liver disease and low portal pressure handle sodium as well as patients with compensated liver disease and high portal pressure. These results are consistent with the notion that in addition to peripheral vasodilatation and severity of liver disease, the severity of portal hypertension contributes to the abnormalities of sodium retention in cirrhosis.     

急性肝衰竭大鼠肠道菌群和内毒素的动态研究

目的 研究急性肝衰竭大鼠肠道菌群及内毒素的动态变化。 方法 腹腔注射半乳糖胺建立急性肝衰竭大鼠模型。40只SD大鼠随机分为A组(对照组)10只;B组12只,C组18只(均为肝衰竭大鼠)。实验开始时(A组)、造模后24 h(B组)和48 h(C组)分别处死各组大鼠并检测肝功能,定性、定量分析空肠、回肠及结肠菌群,定量测定门静脉、右心室血,回肠及结肠内毒素。 结果 肝功能检测显示:B组大鼠的肝脏损伤最为严重;与B组相比,C组大鼠的肝功能开始好转。肠道菌群分析显示:B组大鼠肠道内肠杆菌科细菌显著增加(空肠、回肠间,P<0.01;结肠间,P<0.05)、乳酸杆菌下降(P<0.01);与B组相比,C组空肠和结肠内的肠杆菌科细菌出现下降(P<0.05)、乳酸杆菌增加,以空肠为显著(P<0.05)。内毒素测定表明B组回肠内毒素增加(P<0.05);C组空肠和回肠内毒素继续增高与对照组差异有显著性(P<0.01);门静脉内内毒素在B组最高,与A、C两组比较差异有显著性(P<0.01)。 结论 急性肝衰竭大鼠肠道存在菌群失调、肠杆菌科细菌过度生长,菌群失调程度与肝损伤程度有关;肠道菌群失调伴有回肠和结肠内内毒素升高;门静脉内毒素的增加与肠道菌群失调有关     

腹水超滤浓缩回输腹腔术治疗肝硬化顽固性腹水疗效分析

目的 探讨腹水超滤浓缩回输腹腔术治疗肝硬化顽固性腹水的疗效。方法 将56例肝硬化顽固性腹水患者随机分为2组,均给予保肝、利尿及抗病毒治疗。在此基础上,对治疗组行腹水超滤浓缩回输腹腔术加小剂量人血白蛋白静脉滴注(静滴)(每滤出1000ml腹水,静滴人血白蛋白4g),对对照组行大量放腹水加大剂量人血白蛋白静滴(每抽出1000ml腹水,静滴人血白蛋白8g)。结果 术后第14天,治疗组患者24h尿量、血清ALB水平均高于对照组(P均<0.05),且治疗组总有效率高于对照组(P<0.05)。结论 腹水超滤浓缩回输腹腔术是一种安全有效的治疗肝硬化顽固性腹水的方法。     

Salvianolate inhibits cytokine gene expression in small intestine of cirrhotic rats

AIM:To study the effect of salvianolate on expression of tumor necrosis factor (TNF)-α and interleukin (IL)-6 mRNA in small intestine of cirrhotic rats. METHODS:Cirrhosis in rats was induced using CCl4 (0.3 mL/kg). Rats were randomly divided into non-treatment group,low-dose salvianolate (12 mg/kg) treatment group,medium-dose salvianolate (24 mg/kg) treatment group,and high-dose salvianolate (48 mg/kg) treatment group,and treated for 2 wk. Another 10 healthy rats served as a normal control group. Mortality ...