内镜下曲张血管结扎术对食道曲张静脉破裂出血的预防随机对照研究

目的　食道静脉曲张是门脉高压症 ( PHT)死亡的主要原因 ,预防其出血是治疗门脉高压症的主要目的 ,尽管已经发现心得安对肝硬化 PHT患者曲张静脉第一次出血具有预防作用 ,但由于其副作用 ,禁忌症、非依从性及有治疗失败的报道 ,从而限制了其使用。内镜下曲张静脉结扎术 ( EVL )尚未见用于预防出血。方法　 3 0例有肝硬化门脉高压症患者 ,食道静脉曲张 3～ 4度 ,肝静脉压力梯度≥ 12 mm Hg,无上消化道出血史 ,随机分为 2组 ,一组服用心得安 (将其脉率降低 2 5 % ,15例 ) ,一组行 EVL ( 1～ 2周一次直至曲张血管消失 15例 )。两组进行比…     

用激光多普勒血流仪检测门静脉高压兔的胃粘膜血流量

目的研究门静脉高压症胃粘膜微循环血流量的变化。方法22只兔随机分成2组:门静脉高压模型组(PHT组)11只,通过门静脉部分结扎产生门静脉高压症;假手术组(SO组)11只,仅分离门静脉主干而不结扎。4周后用激光多普勒血流仪(Laser Doppler Flowmetry,LDF)检测胃底、胃窦的粘膜血流量,比较两组间的差异。结果 PHT组胃底、胃窦的粘膜血流量分别为(73.44±25.47)BPU.(97.85±15.05)BPU;SO组相应部位的粘膜血流最为(136.38±18.40)BPU,(89.85±20.34)BPU。PHT组胃底粘膜血流量明显低于SO组(P<0.01),而其胃窦的粘膜血流量与SO组相比稍低,但不具有统计学意义(P>0.05)。结论门脉高压时胃粘膜的血流量降低.     

门静脉高压症外科治疗的新进展

门静脉高压症(PHT)是一组由门静脉系统血流动力学异常和压力持久增高而引起的综合证,是涉及全身多脏器,多系统     

3D DCE MRP在评价肝硬化门脉高压症门静脉系统血管解剖及侧支循环的价值

目的:探讨三维动态对比增强磁共振门脉血管造影(3DDCEMRP)在肝硬化门脉高压症门静脉系统及门体侧支循环显像中的应用价值.方法:对19例肝硬化门脉高压症组病人及51例非肝硬化对照组行3DDCEMRP检查,测量门脉系统各主要干支的径线并比较两者差异;于3DDCEMRP检查前后10d内,对所有肝硬化症组患者行门脉间接造影,以其结果为标准,分析侧支循环发生的部位和分布范围,评价两者的符合情况.结果:肝硬化门脉高压症组MPV、SPV及SMV直径明显大于对照组(P<0.05),门脉分支级数明显减少;但Child A、B级患者间MPV直径及门脉分支级数的减少无明显差别(P>0.05).同时,3D DCE MRP显示2例门脉主干海绵样变并检出48条肝外侧支血管,与DSA结果相对照,除1例脐静脉开放及1例自发性脾肾分流未见显示外,其余侧支循环在3D DCE MRP 上均清楚显影,总符合率为96.0%(48/50).结论:3DDCEMRP能较好显示门脉系统的解剖影像,并对曲张静脉、侧支循环显影良好,也是诊断门脉海绵样变的有效方法.对于门脉高压症的诊断及手术治疗有重要指导意义.     

急诊断流术治疗门脉高压并上消化道出血的研究进展

食管胃底曲张静脉破裂大出血是门脉高压症(门脉高压)的严重并发症,出血来势凶猛,量大,病情危急,迅速有效的止血是改善病人预后的关键.手术治疗是门静脉高压症食管胃底曲张静脉破裂大出血的主要治疗方法,主要有三种:即断流、分流和减少,其术式有数十种之多.本文就断流术治疗门脉高压并上消化道出血的进展做一综述.     

门静脉高压症猪门静脉的生物力学特性及其临床意义

目的:建立猪门静脉高压症模型,探讨门静脉高压症时门静脉的生物力学特性。方法:采用2月龄湖北白种猪,用四氯化碳、苯巴比妥、乙醇,配合高脂、低蛋白、低胆碱饮食进行混合饲养。通过脾静脉插管测压,取门静脉在生物软组织力学试验机上测定其压力-直径关系,横断取材,冰冻切片,H E法染色,用计算机图像分析系统测量其几何形态学指标。结果:实验组门静脉压为(4.17±1.03)kPa,对照组为(1.51±0.79)kPa(P<0.01),实验组门静脉的Einc、Ep和EV均随压力的上升而增大,在相同压力下明显大于对照组的Einc、Ep和EV。在0～4 kPa压力范围内实验组门静脉的顺应性(C)显著低于对照组,而在4～8 kPa的高压时两者顺应性差异并不明显(P>0.05)。结论:门静脉高压症时,门静脉的生物力学特性均发生了明显变化。肝移植时,移植材料间的生物力学特性也应考虑。     

肝内型门脉高压症形成中大鼠门静脉零应力状态的变化

用CCl4注射法制备大鼠肝内型门脉高压模型，通过观察门静脉张开角的大小，研究肝内型门脉高压大鼠在模型建立过程中不同时间点门静脉零应力状态的变化。结果发现，在门脉高压症形成中．大鼠门静脉张开角逐渐增大，从CCl4注射第10周起与对照组相比有显著性差异（P〈0．05）。表明在门脉高压形成过程中，门静脉存在非均匀性生长，门脉高压大鼠门静脉的残余应力和应变大于正常大鼠。     

肝硬化门脉高压症患者胃左静脉组织ET-1和NO的变化与静脉压的关系

目的探讨肝硬化门脉高压症患者胃左静脉组织中内皮素-1(ET-1)和一氧化氮(NO)比值的变化及其与胃左静脉压力的相关性。方法放射免疫法和硝酸酶还原法检测肝硬化门脉高压症患者及对照组患者胃左静脉组织中ET-1和NO含量,术中测定胃左静脉压力,比较两组ET-1/NO比值的变化,并对ET-1/NO比值与胃左静脉压力进行相关性分析。结果门脉高压症患者胃左静脉组织中ET-1/N0比值较对照组明显升高(P<0.05)。ET-1/N0比值与胃左静脉压力呈显著正相关关系(P<0.05)。结论肝硬化门脉高压症患者存在ET-1和NO失衡,ET-1产生相对过多,可能是门脉高压症形成和发展的重要原因之一。ET-1/N0比值与胃左静脉压力相关,可以用来间接反映门静脉压的高低,从而对预测曲张静脉破裂出血有一定的意义。     

血吸虫病性门静脉高压症兔肝脏微血管构筑变化的研究

目的:探讨血吸虫病门静脉高压症时肝脏微血管构筑的变化及其可能在全身高动力循环状态中的作用。方法:采用腹部敷贴法感染血吸虫尾蚴建立血吸虫病性肝纤维化模型,经插管检测心输出量(CO)、平均动脉压(MAP)、心率(HR)和肝静脉嵌塞压(WHVP),按公式计算心脏指数(CI)、外周血管阻力(SVR);通过血管铸型方法观察肝脏微血管构筑。结果:与正常兔比较,血吸虫病兔CO、CI明显增高,MAP和SVR显著降低,WHVP升高,两组间HR差异无统计学意义。肝脏微血管铸型观察,血吸虫病时肝内微血管形态和比例严重失常,肝窦显著膨大,门静脉主干增粗,肝内形成广泛的小吻合支,其间以门静脉终末支与肝静脉终末支、门静脉小分支直接引流入肝静脉多见。结论:血吸虫病性门静脉高压症兔存在肝内门-体分流病理改变,可能是形成全身高动力循环状态并维持门静脉高压的一个重要环节。     

门静脉高压症猪肝动脉的生物力学特性

目的：建立猪门静脉高压症模型,探讨门静脉高压症对肝动脉的生物力学特性的影响。方法：猪以四氯化碳、苯巴比妥、乙醇,配合高脂、低蛋白、低胆碱饮食进行混合饲养。通过脾静脉插管测压,取肝动脉在生物软组织力学试验机上测定其压力-直径关系,计算机图像分析测量肝动脉两端血管环的张开角及其几何形态学指标。结果：实验组门静脉压(4．17±1．03)kPa明显大于对照组(1．51±0．79)kPa,肝动脉的各向同性增量弹性模量、血管容积弹性模量和血管压力-应变模量均随压力的上升而增大,在相同压力下明显大于对照组。肝动脉的顺应性显著低于对照组,而张开角显著增加。结论：门静脉高压症时,肝动脉的生物力学特性发生了显著变化。     

门静脉内皮细胞损伤与门静脉高压症相互关系的研究

采用Masson三色染色法,辅以形态学观察,研究肝硬变病人(n=30)肝内外门静脉的内皮细胞变化。发现血管内皮细胞有明显损伤,伴血栓形成及管壁结构改建。提示血管内皮细胞损伤与门静脉高压症有密切关系。     

门静脉高压家兔胃粘膜损害与胃粘膜血流量及前列腺素的关系

以缩窄家兔门静脉主干制成门静脉高压模型,从组织学、胃壁微循环血液灌注量、胃粘膜前列腺素E_2含量的变化等三个方面探讨了门脉高压对家兔胃壁缺血性改变的影响。结果显示,门静脉高压时胃体、胃底粘膜下层的血液量明显高于正常家兔(P<0.01);血氧饱和度明显低于正常家兔(P<0.01);前列腺素E_2含量亦明显低于正常家兔(P<0.01)。提示,门静脉高压时胃粘膜损害与粘膜下层瘀血、前列腺素E_2含量的降低有关。     

Portal hypertension and schistosomiasis: "an originally killing entity"

In some regions of Africa, Middle-east and Asia, portal hypertension is caused most frequently by bilharziasis far more than by post-hepatic or alcoholic cirrhosis. All schistosomiasis induce hepatic affection, consequence of the eggs embolization in the vessels endings of the portal system, but only Schistosoma mansoni and Asian bilharziasis mainly the Schistosoma japonicum are the cause of severe sequelar fibrosis responsible for a particular portal hypertension. This portal hypertension is original anatomopathologically and physiopathologically. The perivascular concentric fibrosis localised in the portal space is an anatomopathological sequela of bilharzious granulomas outlining embolized eggs. This "stem pipe" aspect constitutes a presinusoidal block inducing a severe portal hypertension without hepatic lobule affection. The recent medical advances regarding this pathology lie in the understanding of the responsible immune mechanisms, the diagnosis and follow-up thanks to ecographic codification of lesions, the complications treatment through varix endoscopic ligature or portal vein derivation. Treatment by praziquantel remains justified together with health education, improving living standard and hopes placed in the future vaccination campaigns associated with medical treatment in endemic areas.     

门脉高压症脾静脉壁的病理改变及组化研究

目的:为了解门脉高压症患者脾静脉壁的病理改变。方法:对15例门脉高压症患者切除脾叶静脉壁进行了普通染色(H.E)和免疫组织化学染色,并以外伤脾为对照,观察其病理改变。结果:15例门脉高压症脾静脉壁均有不同程度的平滑肌肥大、纤维组织增生,13例脾叶静脉壁内皮细胞、脾窦IgG、IgA、C_3、C_4阳性,阳性串为86.7％;10例外伤脾中仅1例阳性,阳性率为10.0％,且无明显的平滑肌肥大和纤维组织增生的改变。结论:门脉高压症患者门静脉系统本身的病理改变以及免疫病理损伤可能影响门脉高压的发生和发展。     

Portal vein or hepatic vein? A curious aberrant vasculature in the liver with idiopathic portal hypertension

The existence of aberrant vasculatures has been described as one of the characteristic findings in the liver with idiopathic portal hypertension (IPH). In this paper, the morphological features and the genesis of aberrant vasculatures were studied on the basis of autopsy and biopsy materials of IPH and animal experiments. Aberrant vasculatures in IPH livers are characterized as thin-walled vessels located mainly adjacent to the portal tracts and at times in the hepatic lobules. Although some of them are morphologically very similar to hepatic vein branches, they are portal in nature. These aberrant vessels develop in order to compensate for portal circulatory insufficiency due to obliteration of portal vein branches, and play an important role in maintaining an adequate blood supply to the parenchyma. It is predicted that decrease of these intrahepatic collateral vessels is responsible for or related to parenchymal atrophy and deterioration of liver function in the advanced stage of this disease. We regard these vasculatures as characteristic of the intrahepatic portal venous obstruction, particularly with portal hypertension accompanied by increased portal blood flow.     

A Case Report of Early Idiopathic Portal Hypertension

We report herein a case (46 years, female) of very early idiopathic portal hypertension. During an examination for in situ uterine cervical cancer, splenomegaly and hypersplenism were incidentally found. CT and MRI showed a nonatrophic liver with dilated portal veins and marked splenomegaly. The portal venous blood flow was increased, while portal venous blood pressure was not high. The spleen (1,220 g) showed hyperplasia of white pulp and congestion. The lobular architecture of the liver was well-preserved, and the subcapsular regions were not atrophic or dropped out. The portal tracts were not fibrotic, and portal veins were neither stenotic nor sclerotic. Instead, lymphoid cell infiltrations were found in about half the portal tracts, and there was subendothelial mononuclear cell infiltration of small portal vein branches. The hepatic lobules showed non-specific reactive change. This case suggests that early hepatic changes recognizable histologically in this disease are lymphoid cell infiltration of the portal tract and of subendothelial regions of portal vein branches, and nonspecific lobular hepatitis. These hepatic changes, as well as marked splenomegaly, may represent an altered immunophenomenon of this disease.     

Phlebosclerotic Colitis in a Cirrhotic Patient with Portal Hypertension: The First Case in Korea

Phlebosclerotic colitis is a rare form of ischemic colitis characterized by the thickening of the wall of the affected colon due to fibrous degeneration of submucosal layer of colon and fibrotic obstruction of the colono-mesenteric vein, resulting in the disturbance of venous return from the colon. The pathogenic mechanism of this entity remains unknown but chronic liver disease with portal hypertension is maybe thought to be one of the speculated mechanisms. Here we first report the case of surgically confirmed phlebosclerotic colitis, that was in the early stage but showed the aggressive nature, in a 61-yr-old cirrhotic patients with portal hypertension in Korea.     

Portal hypertension in chronic hepatitis — Comparative manometric and clinico-chemical examinations

Summary Portal hypertension (PH) which, for patients suffering from chronic liver disease, usually determines their subsequent fate, considerably exceeds the upper limit already in chronic hepatitis. With the aid of laparoscopic transhepatic manometry (LTM) in the branches of the portal and hepatic veins, we measured portal vein pressures of 17.7 and hepatic vein pressures of 12.3 mm Hg in patients with chronic persistent hepatitis (CPH). In patients with chronic aggressive hepatitis (CAH) with still only moderate fibrosis, the pressure was 18.8 (in the portal vein) and 11.0 mm Hg (in the hepatic vein) while in CAH with marked remodelling, the average pressures were 19.9 and 11.8 mm Hg respectively. The early elevation of the PH, also in CPH, is an important indication for a thorough diagnostic work-up and aggressive therapy of the CH.