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1.
刘建军  王吉耀 《肝脏》1999,4(2):84-86
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。  相似文献   

2.
目的 观察肝前性门静脉高压大鼠血中一氧化氮(NO)、碳氧血红蛋白(COHb)与血液循环动力指标的关系。方法 制作门静脉高压大鼠模型和假手术组模型。分别检测血中NO、COHb浓度,测定门静脉压力。血流和平均动脉压。结果 门静脉高压组大鼠血中NO、COHb浓度均较假手术组高,门静脉高压组大鼠门静脉压增高,门静脉血流减少及平均动脉压降低,血中NO、CO-Hb水平分别与门静脉压力呈正相关,与门静脉血流和平均动脉压呈负相关。结论 NO、一氧化碳(CO)的过度形成和释放对门静脉高压的形成和维持起重要作用。  相似文献   

3.
EDRF/NO在门静脉高压症高动力循环中的调节作用   总被引:1,自引:0,他引:1  
EDRF/NO具有舒张血管和调节血液动力学的作用,参与生理和许多病理过程。PHT以心输出量增加、内脏血流量增多、内脏和末稍血管阻力下降为待征的高动力循环状态,并对内源性血管收缩荆反应性下降。近来的研究表明,抑制NO合成可以降低PHT心输出量和内脏血流量,提高血管阻力和对激动荆的反应性,具有改善内脏和全身高动力循环状态。说明在PHT高动力循环发生发展中可能有NO的合成、分泌增多或/和活性增高。NO增多的调节机制尚不清楚。  相似文献   

4.
肝硬化门脉高压症与胃肠动力异常   总被引:4,自引:0,他引:4  
肝硬化门脉高压症可引起食管及胃肠动力异常,而胃肠动力异常又可使肝硬化门脉高压症的病情进一步加剧,甚至导致严重并发症。  相似文献   

5.
血管活性物质与门静脉高压内脏高动力循环   总被引:1,自引:0,他引:1  
内脏高动力循环在门静脉高压发病机制中起着重要作用。而肝硬化时体内血管活性物质紊乱在内脏高动力循环状态的形成中起着主要作用。本文综述了近年来对各种血管活性物质与内脏高动力循环间关系的研究。  相似文献   

6.
胰高血糖素对门静脉高压症影响的研究及进展   总被引:8,自引:0,他引:8  
胰高血糖素的浓度在门静脉高压的病人和动物模型中均有升高,并随着其升高,导致门静脉压力进一步升高。胰高血糖素使胃左静脉离肝血流的发生率和血流速度均明显提高,门脉高压症的食管胃底曲张静脉的管径随之扩大,破裂出血的可能性也因此增加,但曲张静脉对胰高血糖素的反应性随着曲张程度的增加反而下降。只有在门静脉高压存在的条件下,胰高血糖素才会增强乙醇等化学毒性物质对胃粘膜的损伤,这种损伤机制并非因为胰高血糖素造成了胃的高动力循环状态所致,而是与ATP依赖性的K^ 通道有密切的关系。  相似文献   

7.
目的探讨门静脉宽度测量作为评价心得安治疗门脉高压的价值。方法将我院2000—01/2005-01收治的102例肝硬化失代偿期病人随机分成两组,心得安组54例,对照组48例。两组治疗前后分别进行肝功能化验及B超测量门静脉宽度,比较其变化是否有差异。结果心得安组治疗后肝功能改善及门静脉宽度缩小与对照组比较有显著性差异(P〈0.01),提示门静脉宽度测量可作为评价心得安治疗门脉高压疗效的简易指标。  相似文献   

8.
特发性门脉高压症形成的免疫学研究   总被引:1,自引:0,他引:1  
马剑  周霞秋 《肝脏》1999,4(3):167-167
关于特发性门脉高压症(IPH)的病因,历来学者们多从相关脏器如肝脏、脾脏发生的病变进行论述,有多种学说。1891年Banti提出Banti病时认为病因在脾脏,主张脾原说。美国学者认为门静脉末梢血栓形成是门脉高压形成的原因,主张肝原说。日本学者认为单纯以肝脏纤维化、肝内血栓形成或脾肿大、脾血流增加引起门脉高压等单一脏器因素作出IPH病因学解释尚显欠缺,因而提出本病的发生是肝脏、脾脏内皮细胞和淋巴细胞反应的综合结果。近来学者们进行了多项IPH的病因学研究。志方等人发现IPH早期肝细胞浸润和HBsAg…  相似文献   

9.
目的探讨晚期血吸虫病门脉高压症脾切除贲门周围血管离断术后门静脉血栓(PVT)形成的危险因素。方法收集2004年8月至2014年3月期间本院外科收治的211例晚期血吸虫病门静脉高压症患者的临床资料,对可能影响术后PVT形成的因素进行单因素分析和Logistic回归分析。结果 211例患者中,59例术后PVT形成,发生率为27.96%(59/211)。单因素分析显示术前上消化道出血史、门静脉直径、脾静脉直径、食管静脉曲张程度、腹水、门脉高压性胃病、胃底静脉曲张、血氨水平是患者术后PVT形成的影响因素。Logistic回归分析显示门静脉直径增宽(OR=1.763,P=0.000)和门脉高压性胃病(OR=1.089,P=0.037)是患者术后PVT形成的独立危险因素。结论晚期血吸虫病门脉高压症术后PVT形成的发生率较高,门静脉直径增宽和门脉高压性胃病是PVT形成的独立危险因素。  相似文献   

10.
目的研究选择性内皮素受体拮抗剂(内皮素受体A拮抗剂BQ123和内皮素受体B拮抗剂BQ788)对肝硬变门脉高压大鼠血流动力学的影响.方法肝硬变门脉高压大鼠模型由皮下注射四氯化碳诱导,肝硬变大鼠分为肝硬变对照组、肝硬变用药组,分别接受经左心室匀速给予(1 mL·h-1)的生理盐水、BQ123(5和10 nmol·kg-1·min-1),BQ788(10 nmol·kg-1·min-1),BQ123+BQ788(均10 nmol·kg-1·min-1).正常大鼠接受经左心室给予的生理盐水.用药过程中观测大鼠血压和门脉压力的变化情况,用药1 h后应用放射性微球法进行血流动力学测定.结果与正常大鼠相比,肝硬变门脉高压大鼠的动脉血压下降,MAP(17.0±0.37)vs(19.6±0.35)kPa,P<0.01,门脉压上升,PP(1.6±0.04)vs(0.9±0.03)kPa,P<0.01,心指数显著增加,CI(307.3±18.8)vs(163.3±21.9)mL·min-1·kg-1,P<0.01),外周血管阻力(TPR)和内脏血管阻力(PTVR)都下降,TPR(0.1±0.003)vs(0.3±0.04)kPa·mL-1·min-1,P<0.01,PTVR(0.7±0.03)vs(2.1±0.3)kPa·mL-1·min-1,P<0.01,门脉血流量明显增加,PTBF(49.9±4.4)vs(26.0±4.6)mL·min-1·kg-1,P<0.01.接受BQ123 10 mol·kg-1·min-1后,肝硬变大鼠的血压和心率迅速下降,在5min~10min内死亡;接受5 nmol·kg-1·min-1的BQ123时,则表现为MAP下降(3.4±0.7)vs(0.7±0.1)kPa,P<0.01,PP也相应下降(0.1±0.05)vs(0.02±0.01)kPa,P<0.05,CO继续增加(148.9±13.1)vs(113.2±3.8)mL·min-1,P<0.05,TPR有进一步下降的趋势(0.1±0.02)vs(0.1±0.003)kPa·mL-1·min-1,P>0.05,提示高动力循环加重;10 nmol·kg-1·min-1的BQ788可以使PP下降(0.3±0.05)vs(0.02±0.01)kPa,P<0.01,降低肝硬变大鼠的CI(221.0±15.9)vs(307.3±18.8)mL·min-1·kg-1,P<0.01,提高TPR(0.2±0.01)vs(0.1±0.003)kPa·mL-1·min-1,P<0.01,部分纠正了高动力循环和门脉高压.结论肝硬变门脉高压大鼠存在高动力循环状态,BQ123可使其血流动力学状态进一步恶化,BQ788则可部分纠正高动力循环降低门脉压力,这提示ET在维持机体血压和脏器灌注中起重要作用,而由ETA介导的此作用对肝硬变大鼠尤为重要.  相似文献   

11.
特发性门脉高压症的临床病理学特点   总被引:2,自引:0,他引:2  
目的 探讨特发性门脉高压症(idiopathic portal hypertension,IPH)的临床病理学特点.方法 回顾性分析了9例IPH的临床及病理学资料,并对其肝脏标本进行常规病理学及免疫组化研究.结果 9例IPH中,5例首发症状为上消化道出血和黑便,3例体检发现脾大脾亢而无临床症状,1例以血管瘤入院.人院检查脾肿大7例,胃底食道静脉曲张6例,腹水征4例,贫血者6例,肝功能正常或接近正常9例.病理组织学显示9例肝小叶结构基本正常.均未见假小叶形成及肝细胞坏死;9例均有不同程度汇管区纤维化,3例汇管区纤细的不全纤维间隔形成并向肝实质延伸,6例有门脉末支管壁纤维化;9例中有6例小叶内肝细胞有不同程度的水肿变性,5例肝窦有不同程度的扩张,2例肝窦扩张较明显,肝细胞萎缩,呈血管瘤样结构,2例有轻-中度肝腺胞3区大泡脂变.脾脏组织学符合淤血性脾肿大病理表现.结论 IPH的临床表现与其他原因所致的肝硬化门脉高压相似,肝穿组织病理学可除外肝硬化,并有一定的特征.诊断时应与各种原因所致肝硬化门脉高压,肝窦阻塞综合征等相鉴别.  相似文献   

12.
Aneurysmal dilatation of the portal vein (ADPV) is a rare cause of portal hypertension. We described a case of ADPV in a female patient who presented with ascites. Imaging studies revealed tortuosity and dilatation of the main portal vein with turbulent flow. Endoscopy revealed oesophageal varices. A liver biospy showed no abnormalities in liver histology. This is the first case of ascites as a complication of ADPV in the absence of liver cirrhosis, arteriovenous fistula or documented portal vein thrombosis. Hyperdynamic circulation and increased portal vein flow could be implicated in the pathogenesis of ascites in this setting.  相似文献   

13.
Clinical characteristics of idiopathic portal hypertension   总被引:2,自引:0,他引:2  
Idiopathic portal hypertension is one of the interesting causes of portal hypertension. Even in very developed medical centers, this disorder is still one of the most important misdiagnoses of clinical practice. To inexperienced physicians, presenting esophageal varices and upper gastrointestinal bleeding usually prompt an unfortunate diagnosis of cirrhosis. A heterogenous clinical presentation and progression of this disorder should be recognized by physicians, and management should be directed towards some specific problems confined to this disorder. Although a genetic basis and other factors are implicated in its pathogenesis, exact underlying mechanism(s) is (are) unknown. In this review, we discuss the heterogeneity of idiopathic portal hypertension, its etiopathogenesis, clinical presentation and management issues. With the expectation of an excellent prognosis, a practicing gastroenterologist should be aware that "not all varices mean cirrhosis".  相似文献   

14.
AIM: To investigate the role of prostacyclin (PGI2) and nitric oxide (NO) in the development and maintenance of hyperdynamic circulatory state of chronic portal hypertensive rats. METHODS: Ninety male Sprague-Dawley rats were divided into three groups: intrahepatic portal hypertension (IHPH) group by injection of CCI4, prehepatic portal hypertension (PHPH) group by partial stenosis of the portal vein and sham-operation control (SO) group. One week after the models were made, animals in each group were subdivided into 4 groups: saline controlled group (n = 23), Nω-nitro-L-arginine (L-NNA)group (n = 21) group, indomethacin (INDO) group (n = 22) and high-dose heparin group (n = 24). The rats were administrated 1mL of saline, L-NNA (3.3 mg/kg-d) and INDO (5 mg/kg·d) respectively through gastric tubes for one week/then heparin (200 IU/Kg/min) was given to rats by intravenous injection for an hour. Splanchnic and systemic hemodynamics were measured using radioactive microsphere techniques. The serum nitrate/nitrite(NO2-/NO3-) levels as a marker of production of NO were assessed by a colorimetric method, and concentration of 6-keto-PGF1α, a stable hydrolytic product of PGI2, was determined by radioimmunoassay. RESULTS: The concentrations of plasma 6-keto-PGFla (pg/mL) and serum NO2-/NO3- (μmol/L) in IHPH rats (1123.85±153.64, 73.34±4.31) and PHPH rats (891.88±83.11, 75.21±6.89) were significantly higher than those in SO rats (725.53±105.54, 58.79±8.47) (P<0.05). Compared with SO rats, total peripheral vascular resistance (TPR) and spanchnic vascular resistance (SVR) decreased but cardiac index (CI) and portal venous inflow (PVI) increased obviously in IHPH and PHPH rats (P<0.05). L-NNA and indomethacin could decrease the concentrations of plasma 6-keto-PGFla and serum NO2/7NO3-in IHPH and PHPH rats (P<0.05) .Meanwhile, CI, FPP and PVI lowered but MAP, TPR and SVR increased(P<0.05). After deduction of the action of NO, there was no significant correlation between plasma PGI2 level and hemodynamic parameters such as CI, TPR, PVI and SVR. However, after deduction of the action of PGI2, NO still correlated highly with the hemodynamic parameters, indicating that there was a close correlation between NO and the hemodynamic parameters. After administration of high-dose heparin, plasma 6-keto- concentrations in IHPH, PHPH and SO rats were significantly higher than those in rats administrated vehicle (P<0.05). On the contrary, levels of serum NO2-/NO3- in IHPH, PHPH and SO rats were significantly lower than those in rats administrated Vehicle (P<0.05). Compared with those rats administrated vehicle, the hemodynamic parameters of portal hypertensive rats, such as CI and PVI, declined significantly after administration of high-dose heparin (P<0.05), while TPR and SVR increased significantly (P<0.05). CONCLUSION: It is NO rather than PGI2 that is a mediator in the formation and maintenance of hyperdynamic circulatory state of chronic portal hypertensive rats.  相似文献   

15.
Portal hypertension and bleeding from gastroesophageal varices is the major cause of morbidity and mortality in patients with cirrhosis. Portal hypertension is initiated by increased intrahepatic vascular resistance and a hyperdynamic circulatory state. The latter is characterized by a high cardiac output, increased total blood volume and splanchnic vasodilatation, resulting in increased mesenteric blood flow. Pharmacological manipulation of cirrhotic portal hypertension targets both the splanchnic and hepatic vascular beds. Drugs such as angiotensin converting enzyme inhibitors and angiotensin Ⅱ type receptor 1 blockers, which target the components of the classical renin angiotensin system(RAS), are expected to reduce intrahepatic vascular tone by reducing extracellular matrix deposition and vasoactivity of contractile cells and thereby improve portal hypertension. However, these drugs have been shown to produce significant offtarget effects such as systemic hypotension and renal failure. Therefore, the current pharmacological mainstay in clinical practice to prevent variceal bleeding and improving patient survival by reducing portal pressure is non-selective-blockers(NSBBs). These NSBBs work by reducing cardiac output and splanchnic vasodilatation but most patients do not achieve an optimal therapeutic response and a significant proportion of patients are unable to tolerate these drugs.Although statins, used alone or in combination with NSBBs, have been shown to improve portal pressure and overall mortality in cirrhotic patients, further randomized clinical trials are warranted involving larger patient populations with clear clinical end points. On the other hand, recent findings from studies that have investigated the potential use of the blockers of the components of the alternate RAS provided compelling evidence that could lead to the development of drugs targeting the splanchnic vascular bed to inhibit splanchnic vasodilatation in portal hypertension. This review outlines the mechanisms related to the pathogenesis of portal hypertension and attempts to provide an update on currently available therapeutic approaches in the management of portal hypertension with special emphasis on how the alternate RAS could be manipulated in our search for development of safe, specific and effective novel therapies to treat portal hypertension in cirrhosis.  相似文献   

16.
AIM: To study the stability of portal hypertension (PHT) caused by partial ligation of the portal vein ligation (PVL) in a rat model.
METHODS: Thirty male adult Wistar rats were divided into two groups: 10 in Group Ⅰ received a sham operation; and 20 in Group Ⅱreceived partial PVL. Portal vein pressure (PVP) was measured at four time periods: before ligation, 2 wk, 6 wk and 10 wk postsurgery. Portal venography, blood sampling and liver and spleen pathological examinations were conducted at 10 wk after surgery.
RESULTS: The PVP was 9.15± 0.58 cmH2O before ligation, and increased to 17.32 ±0.63 cmH2O 2 wk after PVL. By repeat measurement of the PVP in each rat, it was shown to remain elevated for 10 wk. There were no significant differences in the pressure measurements at 2 wk, 6 wk and 10 wk. Varices were found mainly in the mesenteric vein 2 wk after PVL, which were more obvious later, while these manifestations were similar at week 6 and week 10. Portal venography demonstrated the varices and collaterals. There was no significant change in liver pathology. The volume of the spleen was enlarged 2-fold after ligation, and the sinus of the spleen was enlarged due to congestion. Significant sinus endothelial cell proliferation was observed, but no evidence of hypersplenia was found on hemogram and biochemical examination.
CONCLUSION: These findings suggest that a satisfactory prehepatic PHT rat model can be obtained by partial ligation of the portal vein, and this PHT rat model was stable for at least 10 wk.  相似文献   

17.
Idiopathic portal hypertension (IPH) is a non-cirrhotic presinuosidal portal hypertension of unknown etiology. Stenosis of smaller portal veins with portal fibrosis is a pathologic hallmark of IPH. Association of systemic sclerosis (SSc) with IPH is recognized, and similar pathologic features are reported in small portal tracts and skin of IPH and SSc, respectively. In addition, levels of transforming growth factor-β (TGF-β) and connective tissue growth factor are elevated in serum and in affected skin and portal tracts of these two diseases, suggesting that IPH share fibrogenetic mechanisms with SSc. Endothelial to mesenchymal transition (EndMT) of microvasculatures of skin could be responsible for dermal fibrosis in SSc. In IPH, EndMT of portal vein endothelium via TGF-β/Smad activation may also be involved in small portal venpathy. In IPH, enhanced expression of pSmad2 in venous endothelium of smaller portal veins was associated with reduced CD34 expression. CD34 and S100A4, and CD34 and type I collagen were colocalized to portal vein endothelium in IPH. Such myofibroblastic phenotypes may be responsible for periportal-venous deposition of collagen and compressive portal venous obliteration. These small portal venous lesions may in turn lead to portal venous insufficiency followed by subcapsular atrophy in IPH.  相似文献   

18.
肝硬化是门静脉高压的最常见原因,但仍有约20%的门静脉高压继发于非肝硬化因素,称为非肝硬化性门静脉高压症(NCPH),在发展中国家发病率较高。NCPH是一组异源性的肝脏血管疾病,临床上多见的是特发性门静脉高压(IPH)、肝外门静脉血管阻塞(EHPVO),以及布加综合征、先天性肝纤维化和结节再生性增生等少见病。此类患者常常具有门静脉高压的证据,如反复发生的静脉曲张出血和脾脏肿大,但肝功能保存尚好。目前尚无诊断NCPH的统一标准,对其诊断仍是一个挑战。临床上往往采用排除性诊断,必要时可行肝穿刺活组织检查来确诊。介绍了IPH和EHPVO的发病机制、病理表现、诊断方法及治疗策略的选择,若能有效控制上消化道出血,NCPH被认为是预后相对良好的一类疾病。  相似文献   

19.
BackgroundThe knowledge of natural history of patients with portal hypertension (PH) not due to cirrhosis is less well known than that of cirrhotic patients.AimTo describe the clinical presentation and the outcomes of 89 patients with non-cirrhotic PH (25 with non-cirrhotic portal hypertension, INCPH, and 64 with chronic portal vein thrombosis, PVT) in comparison with 77 patients with Child A cirrhosis.MethodsThe patients were submitted to a standardized clinical, laboratory, ultrasonographic and endoscopic follow-up. Variceal progression, incidence of variceal bleeding, portal vein thrombosis, ascites and survival were recorded.ResultsAt presentation, the prevalence of varices, variceal bleeding and ascites was similar in the 3 groups. During follow-up, the rate of progression to varices at risk of bleeding (p < 0.0001) and the incidence of first variceal bleeding (p = 0.02) were significantly higher in non-cirrhotic then in cirrhotic patients. A PVT developed in 32% of INCPH patients and in 18% of cirrhotics (p = 0.02).ConclusionsIn the patients with non-cirrhotic PH variceal progression is more rapid and bleeding more frequent than in cirrhotics. Patients with INCPH are particularly prompt to develop PVT. This observational study suggests that the management of patients with non-cirrhotic PH should take into consideration the natural history of portal hypertension in these patients and cannot be simply derived by the observation of cirrhotic patients.  相似文献   

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