门脉高压性脾脏多形态结构的实验研究

目的；研究门脉高压性脾脏形态结构。方法；用硫代乙酰胺诱发大鼠门脉高压性脾肿大，不同的时期摘脾研究其形态结构，结果：发现早期脾组织充血水肿８周后红髓区脾窦扩大，脾索狭窄，白髓区动脉周围淋巴鞘萎缩纤维化，形态计量测定表明随着脾肿大的发展，红髓面积百分比增加，白髓面积百分比减少，白髓区内ＰＡＬＳ生发中心面积百分比亦进行性减少；结论：门脉高压性脾脑发挥免疫功能的区域萎缩，其免疫功能低下，此时外科保脾意义不     

血管内皮细胞生长因子mRNA在门脉高压脾脏中的表达

目的 了解血管内皮细胞生长因子mRNA在门脉高压脾脏中的表达。方法 逆转录-聚合酶链反应(RT-PCR)技术检测20例门脉高压小鼠脾脏VEGFmRNA表达。结果 有18例巨脾组织表达VEGF mRNA,表达率为90％;2例无表达。对照组为零。两组间有显著差异(p<0.01).结论 VEGF在门脉高压所致的脾肿大中起重要作用,通过诱导内皮细胞通透性和内皮细胞的增生,促进脾脏的肿大。     

门脉高压食道静脉的解剖结构学特性

食道静脉是门脉高压下最具意义的侧支循环通道，深入研究门脉高压食道静脉的解剖结构学特性，有助于阐明食道静脉曲张出血的病理机制。本文对门脉高压状态食道静脉的整体配布、血液回流、形态构象、组织结构特性的研究现状作了综述。     

部分回结肠切除术治疗门脉高压的实验研究

本文根据门脉系的解剖生理学特点,设计了部分回结肠切除术用以治疗门脉高压症。通过对8只猫的实验观察,表明该术式能有效地降低自由门脉压,缓解门脉压高症,并能在一定程度上提高门脉最大灌注压.本文还将该术式与断流术、分流术进行了比较、讨论。     

脾脏Gaucher病形态结构

患者,男,57岁。因全身乏力伴头晕20年,体检发现脾肿大、全血细胞减少,于1997年10月15日入院。既往有高血压史,否认伤寒、肝炎病史。体检:一般情况良好,皮肤无淤斑及出血点,全身浅表淋巴结不肿大,巩膜无黄染,腹平坦,肝肋下未及,脾肋下8cm,质中等,叩痛(-)。辅助检查:RBC3.1T/L,HGB88g/L,WBC2.5G/L,PLT23G/L,三抗(-),骨髓涂片提示“符合脾功能亢进”,消化道钡餐检查提示“食道静脉轻度曲张”。临床诊断:“脾功能亢进原因待查”。1　病理检查　肉眼观察:巨大脾脏一个,大小25×10×9cm,重3200g,切面呈暗红色。光镜观察:脾小体减少、缩小,…     

门脉高压性肠病组织病理学观察北大核心CSCD

1991年Kozarek等[1]首次提出门脉高压性肠病的概念.指继发于肝门静脉高压以肠道血管扩张为特征的一种病变.包括门脉高压性小肠病和门脉高压性结肠病。门脉高压性肠病的临床和内镜表现已有不少报道,但对病理组织学表现的报道不多[2-3]。我们对存在肝硬化门脉高压的10例结肠活检标本和2例小肠切除标本进行了组织病理学观察。     

门脉高压所致上消化道大出血的内科治疗

门脉高压症是由于门脉血流受阻或血流量异常增多而致的门脉高压为主的一组临床综合症。肝硬化是最常见的病因。食道胃底静脉曲张破裂出血和门脉高压性胃病并发出血,是肝硬化最常见的并发症和死亡原因,也是内科常见的急诊之一。短期内出血量大,来势凶猛,死亡率高达50％以上。内科采用药物止血,气囊压迫止血,以抢救生命。目前我们采用的药物     

EGFR的表达在门脉高压性胃病愈合过程中的作用

目的 EGFR的表达在保护胃黏膜损伤中有重要作用,而在门脉高压性胃病(portal hypertensive gastropathy,PHG)中的作用研究较少.本实验的拟探讨EGFR表达在PHG患者胃黏膜愈合过程中的变化及作用.方法 以10例正常成年人作为对照,根据胃镜检查结果将41例肝硬化门脉高压症患者分成3组,即无PHG患者组8例,轻度PHG患者组18例,重度PHG患者组15例.33例PHG患者给予普萘洛尔治疗,观察愈合情况.研究对象取胃粘膜组织活检,采用酶联免疫法(ELISA)测定胃黏膜EGFR含量.结果 EGFR在轻度PHG胃黏膜表达与正常对照组、无胃病组无显著差异(P ＞0.05),而重度PHG胃黏膜表达正常对照组、无PHG组、轻度PHG组显著降低(P ＜0.01),而在PHG胃黏膜病变好转组中的表达较正常对照组、无PHG组、轻度PHG组、重度PHG显著增多.结论 EGFR在HPG胃黏膜中表达与病变程度相关,并可能在PHG胃黏膜的愈合过程中发挥重要作用.     

门脉高压症巨脾除术的体会

门脉高压症手术治疗中行血管分流手术和/或贲门血管离断术意见虽尚未统一,但术中行脾切除适应症已明确,手术死亡率已明显降低,但广泛血管粘连性的巨脾切除仍相当困难,处理不当合并出血比较凶险。本文就22年以来本院行困难的脾切除的临床资料分析报告如下。 一、临床资料 1.一般情况:1978年6月至2000年6月,本院普外科手术治疗肝硬化所致门脉高压症486例。男353例;女233例。年龄26岁至67岁,平均年龄46岁。肝功能按照Child分级:A级263例,B级176例,C级479例。分流手术237例,断流术217例,分流加断流术18例,脾切除加冠状血管缝扎术14例,术中     

门脉高压大鼠肺微血管周细胞α-SM-actin表达的改变

目的:通过对胆汁性肝硬化门脉高压大鼠肺微血管周细胞α-SM-ac-tin表达的测定,探讨门脉高压肺部微血管是否受累,以及周细胞在其中的作用。方法:实验分为三组:模型组、对照组及治疗组(银杏注射液治疗)。应用结扎胆总管复制胆汁性肝硬化门脉高压模型,采用Masson法、免疫组织化学染色、图像分析等技术研究肝硬化门脉高压对大鼠肺微血管周细胞α-SM-actin表达的影响。结果:模型组平均吸光度0.3499±0.089,对照组平均吸光度0.3344±0.0890,治疗组平均吸光度0.2890±0.102,对三组结果进行两两非配对t检验,均具显著性差异(P0.01)。结论:肝硬化门脉高压可刺激肺微血管周细胞增殖或向平滑肌细胞转化,而银杏注射液能抑制这种改变。这表明门脉高压肺部微血管同样受累,周细胞在病变中可能具有重要的意义。     

Structural characteristic of splenic sinuses in idiopathic portal hypertension

Splenic sinuses in idiopathic portal hypertension (IPH; 8 patients}, liver cirrhosis (LC; 14 patients) and in regenerating autotransplanted spleens from 25 rats were compared with each other by scanning electron microscopy (SEM) and immunohistochemistry using antibodies against proliferating cell nuctear antigen (PCNA). Spleens obtained from six patients with gastric carcinoma and from five untreated adult rats were examined as controls. SEM of the sinuses showed that in IPH endothelial cells became irregular in shape, and the interendothelial slits of sinuses were irregularly entarged. Sinus endothelial processes traversing the sinusal lumen were also found. The same changes were observed in the proliferating sinuses during regeneration of splenic tissue after autotransplantation in rats, but disappeared when the regeneration was completed. Irregular endothelial cells were few in LC. PCNA-positive sinus endothelial cells were increased in number in IPH as compared with those in LC; the mean number of PCNA-positive ones per cm² was 45.4 in IPH and 8.2 in LC. It was suggested that, from SEM observation of sinus endothelial cells and counting PCNA-positive sinus endothelial cells, the sinuses of the spleen in IPH consist of proliferating endothelial cells or are in the state of increased proliferation. In conclusion, splenomegaly in IPH was presumed to be caused by proliferation of sinus endothelial cells, and by the increased splenic blood flow in the irregularly widened interendothelial slits of the sinuses.     

Idiopathic portal hypertension: a histopathological study of 26 Japanese cases

Analysis of 25 liver biopsy specimens and one autopsy specimen from 26 Japanese patients (23 women and three men) with idiopathic portal hypertension revealed findings that collectively appeared diagnostic for the condition. Changes in the portal tract included capillary dilatation, phlebosclerosis, and fibro-elastosis of the stroma. Many portal veins were dilated and had herniated into the surrounding hepatic parenchyma. Portal vein obliteration and loss of bile ducts were a rare complication. The acinar architecture was disturbed by: 1 capillary and necro-infiammatory bridging, mostly between portal tracts and terminal hepatic veins; 2 the formation of isolated megasinusoids in a random distribution; 3 displaced and abnormally large hepatic vein branches with or without phlebosclerosis and 4 slender, curved fibrous septa (hairline septa). Early nodular regeneration was found in 25% of the cases. Our review supports the contention that incomplete septal cirrhosis may be a late manifestation of idiopathic portal hypertension. It is not clear whether the biopsy findings in Japanese patients differ only in severity from those in western patients, or whether the conditions differ pathogenetically. Some histopathological findings in the Japanese cases, in particular the necroinflammatory changes, are difficult to reconcile with portal hypertension as a primary haemodynamic abn rmality.     

A comparative histological and morphometric study of vascular changes in idiopathic portal hypertension and alcoholic fibrosis/cirrhosis

AIM: To examine the pathological changes of hepatic arteries in idiopathic portal hypertension (IPH) which is characterized by the obliteration of the intrahepatic portal vein branches and presinusoidal portal hypertension. METHODS AND RESULTS: Liver specimens (biopsied or surgically resected) from 20 patients with IPH, 20 patients with alcoholic fibrosis/cirrhosis (AF/C) and 20 histologically normal livers were used. The vascular lumina of arterial and venous vessels in portal tracts were morphometrically evaluated by an image analysis system. The ratio of portal venous luminal area to portal tract area (portal venous index) of IPH and that of AF/C were significantly reduced compared with normal liver. The portal venous index for IPH was significantly lower than that for AF/C. The ratio of hepatic arterial luminal area to portal tract area for AF/C was significantly higher than that in normal liver; however, that for IPH was similar to normal. The peribiliary vascular plexus was increased in AF/C but not in IPH. In AF/C, the number of mast cells and macrophages known to be the source of angiogenic substances was significantly increased in the portal tract compared with normal liver, while in IPH it was not increased. CONCLUSIONS: In AF/C, a reduction in portal venous lumen was associated with an increase of hepatic arterial lumen and of angiogenesis-related cells in portal tracts. However, such compensatory arterial changes were not evident in IPH, and this compensatory failure may be a feature of IPH.     

Berry splenic artery aneurysm rupture in association with segmental arterial mediolysis and portal hypertension

A rare case of berry splenic artery aneurysm (SAA) rupture associated with segmental arterial mediolysis (SAM) and portal hypertension is reported. A 66-year-old woman, diagnosed as having liver cirrhosis and portal hypertension 6 years earlier, suddenly developed a lancinating pain in the upper abdomen and lost consciousness. She recovered consciousness while being transferred to hospital by ambulance. During the investigations, her level of consciousness suddenly deteriorated. Ultrasonography showed a massive intraperitoneal hemorrhage, and she died 5(1/2) h after admission. On gross examination at autopsy it was not possible to find the rupture point of the vessel because the pancreas was embedded in a massive hematoma. However, careful dissection of the pancreatic tail after fixation revealed a berry aneurysm measuring 0.8 cm in diameter in a branch adjacent to the bifurcation in the distal third of the main splenic artery. Microscopic examination detected a rupture of the aneurysm. The histology of the arterial wall proximal to the aneurysm showed typical SAM. In general, berry SAA caused by SAM is rare and unlikely to rupture. The SAA in the present case likely occurred and ruptured due to the combination of SAM and portal hypertension.     

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。     

Knockdown of PIK3R1 by shRNA inhibits the activity of the splenic macrophages associated with hypersplenism due to portal hypertension

Phosphatidylinositol 3-kinase (PI3K) plays a central role in the metabolic actions of insulin. One 85 kDa regulatory subunit of PIK3 is encoded by phosphoinositide-3-kinase, the regulatory subunit 1 (PIK3R1). Our previous study has demonstrated that PIK3R1 was up-regulated significantly in the splenic macrophage (MΦ) of portal hypertensive spleen. In the present study, RNA interference specific to PIK3R1 was employed to investigate its inhibitive effects on the activity of MΦ associated with hypersplenism due to portal hypertension (HS-PHT).     

门静脉部分缩窄制作SD大鼠门静脉海绵样变性动物模型

目的采用门静脉部分缩窄法建立SD大鼠门静脉海绵样变性(CTPV)的动物模型,观察成模过程中门静脉压力、门静脉及周围组织的结构变化,为临床及基础研究提供可靠、稳定的模型动物。方法将SD大鼠100只,随机分为2组:假手术组和模型组,每组各50只。模型组用21G口径的钝头针对大鼠门静脉部分缩窄术;假手术组仅对门静脉进行游离探查,不进行缩窄。各组分别在术后1、2、3、4、6w随机取出10只,行门静脉测压、门静脉造影、病理学等观察门静脉及其周围组织侧支循环的形成情况。结果假手术组大鼠术后各时间段均未形成门脉高压,门静脉造影未见有侧支循环形成。模型组术后1w即形成门静脉高压,门静脉造影显示术后第3w,肝门区可见向肝性侧支循环,术后6w,门静脉区形成典型的海绵样变性。结论用21G钝针头行门静脉部分缩窄,可以复制出类似CTPV的大鼠模型。术后3w门静脉压力达到高峰,以后稍有下降并逐渐趋于稳定,在术后3w门静脉已出现向肝性侧支循环,到6w时形成典型的门静脉海绵样变性改变。     

选择性贲门周围血管离断术的临床应用探讨

目的探讨选择性贲门周围血管离断术的临床应用效果。方法回顾性分析我院2010年1月至2013年8月86例肝硬化门脉高压接受断流手术患者的临床资料,按手术方式将其分为选择性断流组和传统断流组,对比2组的手术情况、术后肝功能指标、术后并发症情况。结果选择性断流组手术时间延长,FFP术后降低明显(P0.05),出血量和输血例数2组间无统计学差异(P0.05);选择性断流组术后ALT和AST峰值、并发症发生率均低于传统断流组(P0.05);选择性断流组平均术后住院时间较传统断流组缩短(P0.05)。结论选择性断流术能够更有效降低门静脉压力、减少术后近期并发症,值得临床推广。