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。     

中药防治肝硬化门脉高压的研究进展

门脉高压 ( PHT)是肝硬化常见和危险的并发症。约 70 %的肝硬化患者会出现 PHT和食管静脉曲张 ,其中 30 %有静脉曲张出血的危险。急性出血时 ,死亡率达 40 %～ 5 0 % ,生存的患者中 ,若不经治疗 ,70 %左右迟早会再出血。对肝硬化 PHT除手术和介入治疗外 ,可利用药物降低门脉阻力和减少门脉血流 ,达到减低门静脉压力 ,防治上消化道曲张静脉破裂出血。目前常用的西药主要有 :血管加压素、生长抑素、β-受体阻滞剂、硝基类扩血管药、钙离子拮抗剂、α1-受体阻滞剂或激动剂、利尿剂、5 -羟色胺阻滞剂。NO合成抑制剂硝酸左旋精氨酸、多巴胺…     

肝硬化门脉高压的药物治疗

门脉高工发曲张静脉出血是肝硬化主要死因之一，应用血管活性药物降低门脉压力为控制急性出血的主要措施之一。本文综述近年来有关降门脉压药物研究的进展。     

肝硬化门脉高压发生机理

肝硬化门脉高压症常出现顽固性腹水、胃底与食管静脉曲张破裂出血和肝功能衰竭等严重并发症,因此对其发生机理的认识尤显重要。一、门脉高压的分类和机理以往将门脉高压分为窦前和窦后性,最近有人从血流动力学角度将门脉高压分为流出障碍（门脉系统流出血管阻力增大）和流入增加（流入门脉系统的动脉血流量增加）两大类,具体病因如表１,这一分类使对门脉高压的病因能一目了然。二、肝硬化门脉高压发生机理肝硬化是一种慢性进行性肝病,是门脉高压的最主要病因,其组织病理学有以下特点：（１）弥漫性病变,大体标本可见结节形成;（２）…     

肝硬化门脉血流动力学与一氧化氮、内皮素

探讨肝硬化患者门脉血液动力学与血中 ＮＯ、ＥＴ的相互关系。４８例肝硬化门脉高压患者（代偿期 １８例，失代偿期３０例）及３２例正常人作为研究对象，应用双功多普勒测定门、脾静脉血流量（ＰＶＢＦ＆ＳＶＢＦ），同步测定血中ＮＯ，ＥＴ的水平，分析ＰＶＢＦ、ＳＶＢＦ与ＮＯ、ＥＴ的相关性。门脉系统高血流动力学改变存在于肝硬化门脉高压发病的始终，其形成原因可能在于体内扩血管活性物质ＮＯ的生成增多，及机体对ＥＴ等缩血管物质的敏感性下降，对临床治疗有指导意义。     

软肝冲剂对肝炎肝硬化门脉高压患者血清一氧化氮、内皮素的影响

目的：观察软肝冲剂对肝炎肝硬化门脉高压患者门静脉主干内径及血流量、血流速度和血清一氧化氮（NO），内皮素（ET）的影响。方法：选择肝炎肝硬化门脉高压患者97例，随机分为两组，治疗组口服软肝冲剂，对照级以西药常规治疗，观察治疗后的总有效率、肝功能，门静脉主干内径及血流量、血流速度和血清NO、ET的变化。结果：经治疗后治疗组总有效率优于对照组（P＜0．05），患者ANT，TBil明显降低，Alb和A／G均明显升高，门静脉内径变窄，血流量增多，血流速度变快，同时NO及ET亦显著降低，与对照组比较，差异有显著性意义（P＜0．05或0．01）。结论：软肝冲剂治疗肝炎肝硬化门脉高压疗效显著，能明显改善肝功能，降低门静脉压力，其作用机制之一是降低血清NO、ET水平。     

胰岛素抵抗与肝硬化门脉高压的关系

胰岛素抵抗与疾病发生的关系受到众多学者的关注 ,胰岛素敏感指数是客观反映胰岛素抵抗的指标。肝硬化患者普遍存在高胰岛素血症现象 ,胰岛素抵抗是否与门脉高压的发生有关值得探讨。我们对 46肝硬化患者的胰岛素敏感指数、门脉内径、血流速度、流量、尿钠浓度进行联合测定 ,并与 12例健康对照者比较。现将结果报道如下。对象与方法1.对象 :( 1)肝硬化组 46例 ,均为 1998～ 1999年住院的肝炎性肝硬化患者 ,按Ｃｈｉｌｄ分级 :Ａ级 16例 ,Ｂ级 18例 ,Ｃ级 12例 ,年龄 35～ 72岁 ,平均年龄 5 3岁。 ( 2 )对照组 12人 ,为健康查体者 ,年龄 2 8…     

肝硬化门脉高压症药物治疗的进展

肝硬化门脉高压症药物治疗的进展李绍白（武汉市解放大道５１５号同济医院内科武汉４３００３０）肝硬化门脉高压症（ＰＨＴ）的药物治疗，仍着重于降低门脉压，控制食管、胃底静脉曲张（ＥＧＶ）出血，以及预防首次或再出血。ＥＧＶ急性出血的药物治疗在ＥＧＶ出血者中，...     

肝硬化门静脉高压症的诊断

门静脉高压症是消化系统常见病,指门静脉血流压力增高。肝硬化引起的门静脉高压症患病率高,目前认为由门静脉阻力(R)增加和门静脉血流量(Q)增加所致,肝脏结构改变所致的机械梗阻与神经、体液及代谢因素一同发挥着重要作用。临床表现包括腹腔积液、脾大、侧支循环形成与开放。诊断时须符合以下条件:满足肝硬化及门静脉高压症的诊断,但除外其他病因。     

Effect of laparoscopic splenectomy on portal hypertensive gastropathy in cirrhotic patients with portal hypertension

Aim:  This study investigated the relationship between portal hypertensive gastropathy (PHG) and splenomegaly, and the effect of laparoscopic splenectomy on PHG in cirrhotic patients with portal hypertension.
Methods:  Seventy patients with liver cirrhosis and portal hypertension were prospectively studied. Indication for laparoscopic splenectomy was bleeding tendency in 10 patients, induction of interferon in 45, treatment of hepatocellular carcinoma in seven, and treatment for endoscopic injection sclerotherapy-resistant esophagogastric varices in eight. The severity of PHG was classified into none, mild, or severe according to the classification by McCormack et al. The severity of liver disease was classified using the Child–Pugh score. All patients underwent upper gastrointestinal endoscopy before and 1 month after the operation.
Results:  The prevalence of PHG was significantly correlated with the severity of liver disease using the Child–Pugh score. The severity of PHG was significantly correlated with the resected spleen volume. One month after the operation, PHG was improved in 16 of 17 patients with severe PHG and in 12 of 32 with mild PHG. The Child–Pugh score showed a significant improvement (6.8 ± 1.4 to 6.2 ± 1.2) at 3 months after laparoscopic splenectomy ( P  < 0.0001).
Conclusions:  PHG may be associated with splenomegaly, and laparoscopic splenectomy may have a beneficial effect on PHG, at least for a short time.     

搏动性门脉血泵治疗门脉高压症的实验研究

目的为解决门脉高压症向肝血流减少、肝代谢功能下降及侧支循环压力过高、静脉曲张等问题,我们研制了搏动性门脉血泵,对丝线栓塞性门脉高压模型犬进行门脉外动力泵血的研究.观察入肝血量、肝代谢变化及侧支压力等一系列指标.方法对杂种犬进行门脉左右支丝线栓塞术制备门脉高压动物模型;应用高弹力硅胶球囊连接单流向硅胶瓣"T"型管,制作搏动性门脉血泵;应用强磁场磁极片及低频振荡交流线圈体外提供动力.将血泵"T"管安置于门脉主干前壁侧支平面上,测定血泵工作前后的入肝血流量、侧支静脉压力及吲哚氰绿排泄的变化.结果模型犬血泵平面以上的门脉压力在泵工作后由(30.3±4.2)cm H2O升至(49.0±7.1)cm H2O;入肝血流量由(270±28)ml/min升至(396±25)ml/min;血泵平面以下门脉压由(31.4±3.1)cm H2O降至(18.0±4.3)cm H2O;脾静脉压由(36.2±4.0)cmH2O降至(20.5±3.4)cm H2O;胃底静脉压由(35.3±3.3)cm H2O降至(19.3±4.7)cm H2O;吲哚氰绿排泄率由(0.092±0.009)升至(0.151±0.013);15min滞留率由(19.03±8.50)降至(9.04±2.50).结论搏动性门脉血泵对增加门脉入肝血流,改善肝代谢功能状态及降低侧支压力具有显著作用.血泵结构设计新颖,安置方法合理.动力装置体外固定,易于检修和更换电池,可长期工作.体内部分的长期维护方案正在进一步研究之中.     

骨髓纤维化合并肝硬化门静脉高压1例报告

骨髓纤维化是一种原因不明的造血干细胞异常引起的慢性骨髓增生性疾病,骨髓纤维组织明显增生和髓外造血是骨髓纤维化的病理学基础。其临床进展缓慢,出现进行性贫血、脾脏肿大、外周血幼稚细胞、泪滴状红细胞和骨髓干抽,伴有发热、乏力、盗汗、消瘦等全身症状[1]。临床较少见,大多数在中年以后发病,起病隐匿,临床表现不一,无特异性症状,易误诊、漏诊。本院收治1名骨髓纤维化合并门静脉高压症1例,报道如下。     

Structural and functional changes of the gastric mucosa in rats with portal hypertension

Structural and functional changes of the gastric mucosa were studied in rats made portal hypertensive by partially ligating the portal vein. Studies were carried out at either 3 or 12 days after ligation or sham operation. At 3 days, structural changes were greater than at 12 days, the major effects being vascular congestion in the lamina propria, muscularis mucosa, submucosa, and submucosal oedema. Transmission electron microscopy showed only a mild hyperplasia in the muscularis mucosa. Gastric blood flow appeared to decrease at 3 days post-ligation compared to sham-operated control rats, but was significantly increased by 12 days after ligation (P less than 0.01). Cardiac output also appeared to increase in the portal hypertensive rats by 12 days post-ligation but this was not statistically significant. Portal venous inflow was significantly increased by 12 days (P less than 0.05) but after correction for collateral circulation liver blood flow had returned to normal values by 12 days post-ligation.     

Experimental investigation of the role of endothelin-1 in idiopathic portal hypertension

BACKGROUND AND AIM: The authors' previous report revealed that endothelin-1 might be released from B lymphocytes in cirrhotic patients with hypersplenism. Other investigators have shown that persistent exposure to environmental contaminants including arsenic might induce idiopathic portal hypertension. The aim of this study was to experimentally identify how endothelin-1 is involved in the development of idiopathic portal hypertension and which cells produce endothelin-1 in the spleen. METHODS: Portal pressure and venous endothelin-1 concentrations were measured in rats that were given sodium arsenate orally for long periods, and endothelin-1 expression levels in the spleen were assessed by staining. In a second experiment, B and T lymphocytes and monocyte-derived macrophages cultured from healthy human peripheral blood were stimulated with sodium arsenite, sodium arsenate, lipopolysaccharide and interferon-gamma. Endothelin-1 concentrations in the supernatants were measured by ELISA. RESULTS: Arsenic exposure gradually increased portal pressure and venous endothelin-1 levels in rats. Endothelin-1 concentration in the supernatant did not change in every cell type stimulated with arsenic, but it increased in B lymphocytes and monocyte-derived macrophages treated with lipopolysaccharide and interferon-gamma. CONCLUSIONS: The in vivo study indicated that arsenic might elevate portal pressure through mechanisms involving endothelin-1. In the in vitro study, lipopolysaccharide and interferon-gamma clearly induced endothelin-1 synthesis not only in monocyte-derived macrophages but also in B lymphocytes, although arsenic treatment did not affect those cells. This study partially supports the hypothesis that idiopathic portal hypertension might be promoted by endothelin-1 overproduction from splenic B lymphocytes in response to certain substances.     

Frequency and factors influencing portal hypertensive gastropathy and duodenopathy in cirrhotic portal hypertension

Portal hypertensive gastropathy and duodenopathy are distinct clinical and endoscopic entities. Data on factors influencing the development of these lesions are still emerging. Data on portal hypertensive duodenopathy are scarce. We prospectively studied 230 patients with liver cirrhosis and oesophageal varices attending the liver clinic of the Sanjay Gandhi Post Graduate Institute of Medical Sciences. One hundred and forty-two patients had no history of upper gastrointestinal bleeding, while the remainder had bled in the past. Endoscopic appearances were recorded before starting patients on a sclerotherapy programme. Forty-four patients were re-evaluated after variceal eradication. The frequency of portal hypertensive gastropathy (PHG) and duodenopathy (PHD) was 61 and 14%, respectively. Mild PHG was present in 85% and was severe in the rest. Portal hypertensive duodenopathy was mild in 50%, while in the other half it was severe. There was no relationship of PHG and PHD to: (i) a history of upper gastrointestinal bleed; (ii) size of oesophageal varices; (iii) aetiology of liver cirrhosis; or (iv) liver function status as assessed by Child Pugh's scores (P=NS for all). The prevalence of PHG was higher in those patients with oesophagogastric varices (74 of 107; 69%) compared with patients with oesophageal varices alone (68 of 123; 55%; P<0.05). However, no such increase in frequency of PHD was noted in patients with oesophagogastric varices. Sclerotherapy increased the frequency of PHG. Twenty-four patients had PHG before starting sclerotherapy, while it was noted in 33 patients 1–3 months after variceal eradication (P< 0.05). In contrast, there was no increase in the prevalence of portal hypertensive duodenopathy after sclerotherapy (P=NS). There was no correlation between endoscopic and histological changes of PHG and PHD. In conclusion, PHG is quite frequent in patients with cirrhosis and its frequency increases with the presence of oesophagogastric varices and after sclerotherapy. However, the frequency of PHD is low and is not affected by the factors studied.     

大鼠肝前型门脉高压症形成中门静脉结构的动态变化

目的探讨大鼠肝前型门脉高压症形成中门静脉血管结构的动态变化及意义。方法以部分门静脉结扎（PVL）法复制肝前型门脉高压症大鼠模型，采用组织形态学方法及计算机图像分析技术测定PVL术后1、2、4、8、12、16、20、26天大鼠的门静脉内径（ID）、外径（OD）、壁厚（WT）、壁面轵（CSA）及平滑肌含量（SMC），同步监测大鼠门静脉压力（PVP）、门静脉血流量（PVF）、平均动脉压（MAP）、门静脉阻力（PVR）、内赃血管阻力（SVR）等血液动力学参数的动态变化。结果PVL术后，大鼠的PVP、PVR、SVR、MAP发生了显著变化。PVL大鼠门静脉CSA从术后12d起，ID、OD、WT和SMC从术后16d起较对照组显著增加（P〈0．05）。结论门脉高压大鼠存在高动力循环状态（HCS）。HCS可引起门静脉结构变化，其管壁增厚，内外管径增大，平滑肌增生。     

Protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats

Objective:To observe the protective effect of omeprazole on gastric mucosal of cirrhotic portal hypertension rats.Methods:All rats were randomly divided into normal control group,cirrhosis and treatment group.Thioacetamide was used to establish rat model of cirrhotic portal hypertension.The necrotic tissue of gastric mucosa ulcer focus,degree of neutrophils infiltration at the ulcer margin,portal pressure,portal venous flow,abdominal aortic pressure,abdominal aortic blood flow at front end,gastric mucosal blood flow(GMBF),glycoprotein(GP)of gastric mucosa,basal acid secretion,H' back-diffusion,gastric mucosal damage index,NO,prostaglandin E_2(PGE_2) and tumor necrosis factor-α(TNF-α) were determined respectively,and the pathological changes of gastric mucosa were also observed by microscope.Results:Compared with cirrhosis group and the control group,the ulcer bottom necrotic material,gastric neutrophil infiltration and UI of the treatment group were all decreased significantly(P0.01),GMBF value,GP values,serum NO,PGE_2,TNF- a were all significantly increased.Conclusions:Omeprazole has an important protective effect on gastric mucosal and it can increase gastric mucosal blood flow and related to many factors.