门静脉高压症患者脾静脉壁细胞间黏附分子-1激活的意义

目的 研究蛋白激酶Cα（PKCα）和细胞间黏附分子-1（ICAM-1）在门静脉高压症患者脾静脉血管的表达，探讨其在门静脉高压症形成机制中的作用。方法 对34例门静脉高压症患者的脾静脉与30例对照组织行ICAM-1原位杂交染色。用逆转录-聚合酶链反应（RT—PCR）测定门静脉高压症患者脾静脉血管平滑肌细胞（VSMC）中PKCα mRNA的表达。结果 正常脾静脉I—CAM-1原位杂交染色呈阴性或弱阳性。门静脉高压症患者脾静脉呈强阳性，差异有统计学意义（P〈0．01）。RT—PCR表明门静脉高压症患者脾静脉VSMC中PKCα mRNA的表达是正常的2．81倍。结论 PKCa和ICAM-1过度表达可能是门静脉高压症患者肝外血管结构改变的重要原因；I—CAM-1的激活在门静脉高压症的形成机制中有重要作用。     

细胞外信号调节激酶1/2及c-fos在门静脉高压症患者脾静脉壁的表达及意义

目的探讨丝裂原激活蛋白激酶(MAPK)信号传导通路是否参与门静脉高压性血管病变的发生过程.方法实验组为乙肝后肝硬化门静脉高压症患者18例,住院期间行择期脾切除加贲门周围血管离断术.对照组选取同期因外伤性脾破裂急诊入院行脾切除术患者10例.采用Western blot方法检测脾静脉组织总蛋白中磷酸化细胞外信号调节激酶丝裂原ERK1/2的表达.采用免疫组织化学方法观察c-fos在脾静脉组织中的表达情况.结果实验组脾静脉壁ERK1/2活性较正常组明显增高(P<0.01).实验组脾静脉壁c-fos表达增高,平均染色指数为6.267 5±0.312 4,正常组脾静脉壁c-fos表达增高,平均染色指数为1.821 3±0.504 1,两者比较差异有统计学意义(P<0.01).c-fos在平滑肌细胞中强阳性表达.结论 ERK1/2/c-fos信号传导途径与门静脉高压性血管病变的发生有关,ERK1/2/c-fos信号传导途径可能是血管平滑肌细胞表型转变的重要调控途径.     

肝硬化患者脾静脉和胃冠状静脉壁类粥样硬化样改变

研究肝硬化门静脉高压症患者脾静脉和胃冠状静脉壁类粥样硬化样改变,并探讨其发生机理及临床意义。方法５０例肝硬化门静脉高压症患者,在行脾切除贲门周围血管离断术时取一段脾静脉和胃冠状静脉供研究,１０例十二指肠球部溃疡患者和１０例外伤性脾破裂患者为对照组,行光镜和电镜观察。     

肝硬变门静脉高压症患者血红素氧化酶-1的表达

目的　探讨肝硬变门静脉高压症患者脾脏及脾血管血红素氧化酶 (HO ) 1mRNA的表达。方法　应用原位杂交方法检测 2 0例肝硬变门静脉高压症患者脾脏、脾动脉、脾静脉组织HO 1mRNA的表达 ,以 12例脾破裂患者作对照。结果　对照组仅有 4例脾组织可见弱阳性表达 ,平均阳性染色指数为 0 .0 5± 0 .0 1,其脾动、静脉组织未见HO 1mRNA表达。肝硬变门静脉高压症组 18例脾脏HO 1mRNA阳性表达 ,平均阳性染色指数为 0 .68± 0 .12 ,显著高于对照组 (P <0 .0 0 1)。脾动、静脉HO 1mRNA全部表达者 15例 ,脾动、静脉阳性染色指数分别为 0 .5± 0 .1与 0 .5 6± 0 .1,两者差异无显著性 ,(P >0 .0 5 )。结论　肝硬变门静脉高压症合并多种应激原刺激患者HO 1mRNA表达增强 ,HO 1及其代谢产物可能参与门静脉高压症多种病理过程。     

门静脉高压症脾切除术中脾静脉近端结扎预防门静脉血栓的疗效分析

目的 探讨门静脉高压症脾切除术中行脾静脉近端结扎对脾静脉源性门静脉血栓的预防效果.方法 回顾性分析2014年8月至2019年7月宁夏回族自治区人民医院手术治疗的94例门静脉高压症患者的临床资料,其中36例行贲门周围血管离断术和脾切除联合经脾静脉冠肾静脉分流术的患者采取紧贴门静脉结扎脾静脉的方法,58例未行脾静脉结扎的贲...     

局部血管紧张素Ⅱ水平与核因子-κB、p38丝裂素活化蛋白激酶信号传导通路活化在人门静脉高压症脾静脉血管病变中的作用

目的 探讨血管紧张素Ⅱ(AngII)与核因子(NF)-κB、p38丝裂素活化蛋白激酶(p38MAPK)信号传导通路活化在人门静脉高压症(PHT)脾静脉血管病变中的作用及其机制.方法 PHT组为乙肝后肝硬化门静脉高压症患者26例;对照组选取因外伤性脾破裂行脾切除术患者10例.放免法(RIA)检测脾静脉中AngII水平;免疫组织化学法测定脾静脉中NF-κB、Phospho-p38蛋白的表达.蛋白免疫印迹法检测脾静脉及体外培养的脾静脉血管平滑肌细胞的NF-κB 、Phospho-p38蛋白的表达.结果 PHT组脾静脉组织AngII为(248.91±48.31)ng/L,显著高于对照组AngII为(143.35±36.45)ng/L(P<0.01).免疫组织化学和蛋白免疫印迹均显示PHT组脾静脉NF-κB 、Phospho-p38蛋白的表达较对照组明显增强.体外培养脾静脉血管平滑肌细胞(VSMC),AngII在1×10-8～1×10-6mol/L浓度范围内,AngII以浓度依赖性方式增加人脾静脉VSMC中NF-κB 、Phospho-p38蛋白的表达.结论 门静脉高压症时脾静脉组织AngII水平升高,NF-κB、Phospho-p38蛋白表达增加.AngII能激活脾静脉血管平滑肌细胞NF-κB、p38信号传导通路.门静脉高压症时AngII可能通过激活P38和NF-κB信号对传导通路门静脉高压症的形成和维持可能起重要作用.     

细胞间粘附因子-1在门静脉高压患者脾静脉的表达及意义

目的 探讨细胞间粘附因子—1(ICAM—1)在门静脉高压患者脾静脉的表达及其在贲门周围血管离断术后门静脉血栓形成的意义。方法 对34例门静脉高压患者和34例单纯脾破裂患者的脾静脉行苏木素—伊红染色观察形态学变化；行ICAM—1原位杂交并行定量分析，术后观察门静脉血栓的发生，对两者的关系进行研究。结果 门静脉高压患者脾静脉中膜平滑肌增生，内膜增厚，门静脉高压组和脾破裂组之间脾静脉内皮细胞ICAM—1mRNA表达差异有非常显著性(P＜0．01)；脾破裂组术后无门静脉血栓形成，门静脉高压组有8例门静脉血栓形成；门静脉高压组内有无门静脉血栓形成病例之间脾静脉内皮细胞ICAM—1mRNA表达差异有显著性(P＜0．05)。结论 门静脉高压性血管病变及其内皮细胞ICAM—1mRNA过度表达可能是门静脉高压患者门静脉血栓形成重要原因。     

门静脉高压症患者脾静脉平滑肌细胞gax mRNA的表达

目的观察门静脉高压症患者脾静脉平滑肌细胞gax mRNA的表达。方法应用逆转录-聚合酶链反应(RT-PCR)和免疫组织化学法分别检测28例门脉高压症患者脾静脉和12例正常对照血管gax mRNA和PCNA蛋白的表达。结果gax mRNA在实验组和对照组中相对表达量分别为1.13±0.21和10.17±0.81(P<0.01);PCNA蛋白在实验组中的表达为(29.8±4.7)%,而正常对照组无明显表达(P<0.01)。结论门静脉高压症患者脾静脉平滑肌细胞中gax mRNA表达下降PCNA蛋白过表达,调节了脾静脉平滑肌细胞增殖、迁移和表型改变,使血管结构重建,对门静脉高压症的形成和维持可能起重要作用。     

贲门周围血管离断术后门静脉血栓形成机制的研究

目的 探讨门静脉高压症患者行贲门周围血管离断术后门静脉血栓形成的机制。方法 对34例门静脉高压患者和34例单纯脾破裂患者的脾静脉行HE染色观察形态学变化，行免疫组化染色并定量分析。结果 门静脉高压患者脾静脉中膜平滑肌增生，并发生玻璃样变，内膜增厚。站静脉高压组和脾破裂组之间脾静脉内皮细胞间粘附因子（ICAM）－1表达差异有显著意义（P＜0．01）。脾破裂组术无门静脉血栓形成，门静脉高压组有8例门静脉血栓形成。门静脉高压组有无门静脉血栓形成病例之间脾静脉内皮细胞ICAM－1表达差异有显著意义（P＜0．05）。结论 门静脉高压血管病变及其内皮细胞ICAM－1过度表达可能是门静脉高压患者门静脉血栓形成的重要原因。     

直接门静脉造影在门静脉高压症治疗中的作用

目的 研究直接门静脉高压症治疗中的作用。方法 采用直接门静脉造影观察１８５例门静脉高压症患者例支血管和冠状静脉解剖,根据造影结果对３５例门静脉高压症患者行经腹联合门奇断流术。结果 门静脉高压症患者显示冠状静脉２２３支,其中单支７９．４６％,双支２０．５４％,冠状静脉开口于门静脉主干、脾静脉和门脾静脉交汇处分别为６２．３３％、２７．３５％和８．０７％,出血和断流术后现出知患者主要位于门静脉主干,顽固     

门静脉高压症患者肝外血管平滑肌细胞增生与c-myc基因表达的相关性研究

目的　研究门静脉高压症患者肝外血管平滑肌细胞增生与c mycmRNA表达的关系。方法　应用RT PCR和免疫组化法对 2 8例门静脉高压症患者的脾静脉、12例正常血管分别进行c mycmRNA和增殖细胞核抗原 (PCNA)的检测。结果　门静脉高压症患者脾静脉PCNA蛋白表达阳性指数为 (2 9 8± 4 2 ) % ;c mycmRNA在PCNA蛋白表达阳性组和阴性组分别为 (7.6 1± 1 0 4 ) %和(3 82± 0 92 ) % ,正常对照组血管中PCNA蛋白无表达、c mycmRNA表达为 (1 0 4± 0 2 1) % ,两者同时与对照组比较 ,差异有显著意义 (P <0 0 1)。结论　c myc基因是门静脉高压症患者肝外血管平滑肌细胞增殖的起动基因 ,门静脉血流动力学紊乱激活脾静脉壁平滑肌细胞中原癌基因 ,促使血管平滑肌细胞增殖、迁移和表型改变 ,导致脾静脉血管重塑 ,使血管对缩血管物质反应降低。     

静脉高压对大隐静脉和脾静脉管壁细胞形态学的影响

目的探讨静脉高压对大隐静脉和脾静脉管壁细胞形态的影响。方法分别收集曲张大隐静脉(20例)、门静脉高压性脾静脉管壁(14例)、正常大隐静脉(8例)和正常脾静脉(6例)标本,制作切片在电镜下观察其形态。结果电镜下曲张性大隐静脉和高压性脾静脉管壁均出现内皮细胞线粒体变性,平滑肌细胞胞浆内粗面内质网、核糖体、线粒体等细胞器增多,肌丝减少等改变。结论静脉高压影响曲张性大隐静脉和高压性脾静脉管壁细胞形态学的重塑,二者的改变是相同的。     

选择性脾胃区减断分流术后血流动力学变化的实验研究

目的 研究门静脉高压症犬行选择性脾胃区减断分流术(selective decongestive devascular-ization shunt of gastrosplenic region,SDDS-GSR)后血流动力学变化.方法 用正常犬制备门静脉高压脾亢模型并进行SDDS-GSR术.制模前、成模后,分流术后30 d和术后60 d观察门静脉压力,门静脉、肝动脉、脾静脉和脾动脉的内径、血流速度和血流量参数的变化,作自身对照研究.结果 SDDS-GSR术后30 d的脾胃区静脉压力显著下降(P<0.01),门静脉、脾动脉和脾静脉内径显著缩小(P<0.01),门静脉、脾动脉和脾静脉血流量参数减少(P<0.01),肝动脉内径和血流量参数显著增加(P<0.01),术后60 d上述指标改变仍保持稳定.结论 sDDS-GSR术通过减少脾动脉血流和改善脾静脉回流,有效地降低了脾胃区的静脉压力,并保持肠系膜区的相对高压,同时增加肝动脉向肝血流量,保证了门脉的向肝血流量,术后血流动力学变化较持久稳定,是一种合理而可取的治疗门静脉高压症的术式.     

高血流动力对大隐静脉和脾静脉血管重塑的影响

目的探讨高血流动力对大隐静脉和脾静脉血管重塑的影响.方法收集曲张大隐静脉和门静脉高压性脾静脉管壁标本34例,设正常大隐静脉和脾静脉14例为对照组,光学显微镜下观察HE染色和Masson染色后的大隐静脉、脾静脉管壁组织学改变.结果 HE染色曲张大隐静脉管壁呈不均匀性增厚改变,高压性脾静脉呈均匀性增厚改变;Masson染色管壁增厚,以内膜、中膜肌层和纤维结缔组织增生为主,曲张的大隐静脉（2/20）内膜轻度黏液样变性,高压性脾静脉（5/14）重度黏液性变性.结论高血流动力学影响大隐静脉和脾静脉管壁的重塑,提示内脏静脉比外周静脉病理改变更明显.     

Isolated Gastric Varices Resulting from Iatrogenic Splenic Vein Occlusion: Report of a Case

Iatrogenic splenic vein occlusion is known to be a rare cause of left-sided portal hypertension. We herein describe the clinical course of a 43-year-old woman with isolated gastric varices, which proved to be attributable to a segmental splenic vein resection during an operation for a benign pancreatic tumor 11 years previously. Seven years after the initial operation, prominent gastric varices due to left-sided portal hypertension were first noted. During the follow-up period of 4 years, she had no episodes of gastrointestinal hemorrhaging. Although the size of the gastric varices did not change, she decided to have a splenectomy considering the potential risk of variceal hemorrhaging. It may be reasonable to perform a splenectomy concomitantly when the splenic vein is to be resected or ligated during pancreatic surgery to avoid the future development of left-sided portal hypertension. However, the role of prophylactic surgery in asymptomatic patients with iatrogenic splenic vein occlusion remains to be determined. Received: June 3, 2002 / Accepted: November 19, 2002 RID="*" ID="*" Reprint requests to: Y. Ku     

Left-sided portal hypertension: Successful management by laparoscopic splenectomy following splenic artery embolization

INTRODUCTION

Left-sided portal hypertension is a rare clinical condition most often associated with a pancreatic disease. In case of hemorrhage from gastric fundus varices, splenectomy is indicated. Commonly, the operation is carried out by laparotomy, as portal hypertension is considered a relative contraindication to laparoscopic splenectomy (LS). Although some studies have reported the feasibility of the laparoscopic approach in the setting of cirrhosis-related portal hypertension, experience concerning LS in left-sided portal hypertension is lacking.

PRESENTATION OF CASE

A 39-year-old man was admitted to the Emergency Department for haemorrhagic shock due to acute hemorrhage from gastric fundus varices. Diagnostic work up revealed a chronic pancreatitis-related splenic vein thrombosis causing left-sided portal hypertension with gastric fundus varices and splenic cavernoma. Following splenic artery embolization (SAE), the case was successfully managed by LS.

DISCUSSION

The advantages of laparoscopic over open splenectomy include lower complication rate, quicker recovery and shorter hospital stay. Splenic artery embolization prior to LS has been used to reduce intraoperative blood losses and conversion rate, especially in complex cases of splenomegaly or cirrhosis-related portal hypertension. We report a case of complicated left-sided portal hypertension managed by LS following SAE. In spite of the presence of large varices at the splenic hilum, the operation was performed by laparoscopy without any major intraoperative complication, thanks to the reduced venous pressure achieved by SAE.

CONCLUSION

Splenic artery embolization may be a valuable adjunct in case of left-sided portal hypertension requiring splenectomy, allowing a safe dissection of the splenic vessels even by laparoscopy.     

Pathological abnormalities in splenic vasculature in non-cirrhotic portal hypertension:Its relevance in the management of portal hypertension

BACKGROUND Portal hypertension(PH) is associated with changes in vascular structure and function of the portosplenomesenteric system(PSMS).This is referred to as portal hypertensive vasculopathy.Pathological abnormalities of PSMS has been described in the literature for cirrhotic patients.Raised portal pressure and hyperdynamic circulation are thought to be the underlying cause of this vasculopathy.In view of this,it is expected that pathological changes in splenic and portal vein similar to those reported in cirrhotic patients with PH may also be present in patients with non-cirrhotic PH(NCPH).AIM To investigate pathological abnormalities of splenic vein in patients with NCPH,and suggest its possible implications in the management of PH.METHODS A prospective observational study was performed on 116 patients with NCPH[Extrahepatic portal vein obstruction(EHPVO):53 and non-cirrhotic portal fibrosis(NCPF):63] who underwent proximal splenorenal shunt(PSRS),interposition shunt or splenectomy with devascularization in JIPMER,Pondicherry,India,a tertiary level referral center,between 2011-2016.All patients were evaluated by Doppler study of PSMS,computed tomography portovenogram and upper gastrointestinal endoscopy.An acoustic resonance forced impulse(ARFI) scan and abdomen ultrasound were done for all cases to exclude cirrhosis.Intraoperative and histopathological assessment of the harvested splenic vein was performed in all.The study group was divided into delayed and early presentation based on the median duration of symptoms(i.e.108 mo).RESULTS The study group comprising of 116 patients [77(66%) females and 39(34%)males] with NCPH had a median age of 22 years.Median duration of symptoms was 108 mo.The most common presentation in both EHPVO and NCPF patients was upper gastrointestinal bleeding(hematemesis and melena).The ARFI scan revealed a median score of 1.2(1.0-1.8) m/s for EHPVO and 1.5(0.9-2.8) m/s for NCPF.PSRS was performed in 84 patients(two of whom underwent interposition PSRS using a 10 mm Dacron graft);splenoadrenal shunt in 9;interposition mesocaval shunt in 5;interposition 1 st jejunal to caval shunt in 1 patient and devascularization with splenectomy in 17 patients.Median presplenectomy portal pressure was 25(range:15-51) mm Hg.In 77% cases,the splenic vein was abnormal upon intraoperative assessment.Under macroscopic examination,wall thickening was observed in 108(93%),venous thrombosis in 32(28%) and vein wall calcification in 27(23%) cases.Upon examination under a surgical magnification loupe,21(18%) patients had intimal defects in the splenic vein.Histopathological examination of veins was abnormal in all cases.Medial hypertrophy was noted in nearly all patients(107/116),while intimal fibrosis was seen in 30%.Ninety one percent of patients with intimal fibrosis also had venous thrombosis.Vein wall calcification was found in 22%,all of whom had intimal fibrosis and venous thrombosis.The proportion of patients with pathological abnormalities in the splenic vein were significantly greater in the delayed presentation group as compared to the early presentation group.CONCLUSION Pathological changes in the splenic vein similar to those in cirrhotic patients with PH are noted in NCPH.We recommend that PH in NCPH be treated as systemic and pulmonary hypertension equivalent in the gastrointestinal tract,and that early aggressive therapy be initiated to reduce portal pressure and hemodynamic stress to avoid potential lethal effects.     

脾动脉缩窄式远端脾肾分流术七例

目的 探讨脾动脉缩窄式(splenic artery coarctation，SAC)远端脾肾静脉分流术(USRS-SRC)治疗门脉高压症的疗效。方法 7例肝硬化门脉高压症病人行DSRS-SAC术，术后随访3～11个月。术前和术后观察门静脉压力、门静脉直径和脾脏大小变化，以及外周血细胞计数、肝功能的改变。结果 DSRS-SAC术后脾胃区静脉压力明显下降(P＜0．01)，又能维持良好的向肝血流灌注，脾脏显著缩小（P＜0．01)，脾亢纠正，无肝性脑病和再出血。血清总胆红素升高(P＜0．05)，3例腹水一度增多。结论 DSRS-SAC是一种治疗门脉高压症可选择的较理想术式。     

Significance of splenic vein thrombosis in chronic pancreatitis

BACKGROUND: Splenic vein thrombosis leading to sinistral portal hypertension and variceal bleeding is a complication of chronic pancreatitis. The management of these patients without variceal bleeding remains controversial. METHODS: A total of 157 patients with chronic pancreatitis were managed consecutively in our center between January 1996 and December 2005. Thirty-four patients with chronic pancreatitis were diagnosed to have splenic vein thrombosis. RESULTS: The incidence of splenic vein thrombosis in patients with chronic pancreatitis was 22%. Fifteen percent of patients with chronic pancreatitis and splenic vein thrombosis presented with gastroesophageal variceal bleeding. Nine patients underwent splenectomy along with pancreatic procedures and 21 patients underwent pancreatic procedures only. Adding splenectomy to the pancreatic procedure did not lead to increased morbidity or mortality. CONCLUSION: Splenectomy should be added to the pancreatic procedure in patients who have evidence of portal hypertension on preoperative evaluation, especially if gastric varices are found.     

三联手术治疗小儿肝外门静脉高压

目的评价脾肺固定术 断流术 脾动脉结扎术治疗小儿门脉高压的疗效. 方法 1993年3月～1998年11月对7例确诊为门脉高压的患儿行三联手术治疗.测定手术前后白细胞、血小板计数和肝功能,脾动脉结扎前后游离门静脉压.术后随访2～8年,平均5.6年.记录上消化道出血的发生情况,并采用钡餐评定食管胃底静脉曲张的程度.B超测定脾脏和门静脉直径,以彩色多普勒血流显像测定门肺分流及门静脉血流,粘度计行血液流变学检测.结果本组无手术死亡.术后食管及胃底曲张静脉的出血被完全控制.白细胞及血小板计数恢复至正常水平,脾脏直径进行性缩小.静脉曲张趋于缓解,游离门静脉压由术前(42.62±6.72) cm H2O降至术后(34.48±5.71) cm H2O,差异有统计学意义(P＜0.05).门静脉血流量亦降低,其血流方向至肝;脾静脉血流方向至脾.术前全血粘滞度降低,术后恢复至正常水平. 结论三联手术可有效地控制肝外门脉高压由于静脉曲张导致的出血.