Morphological changes of blood spleen barrier in portal hypertensive spleen

The pathogenesis of hypersplenism and the immune function of the spleen in patients with portal hypertension （PH） remain obscure. This study aimed to evaluate the morphological changes of blood spleen barrier in spleen with hypersplenism due to PH and provide evidence for an in-depth investigation of the immune function of the spleen with hypersplenism and the mechanism of hypersplenism. Methods Spleen samples from 12 portal hypertensive patients and 4 patients with traumatic ruptures of spleen were examined. The samples of spleen were made into pathological sections, stained with Masson trichrome stain, Gomori stain, and CD68, CD34 immunohistochemistry, and were examined microscopically for the changes in the distribution of collagen fibers, reticular fibers, macrophages, and vascular endothelial cells. The changes in ultrastructure of macrophages and endothelial cells in marginal zone were also evaluated by transmission electron microscopy. Results As compared to the normal spleen, the density of macrophage in the PH spleen was decreased, but the macrophages were mainly located in the marginal zone and distributed around the splenic corpuscle, with many villi and pseudopodium-like protrusion on the cell surface. The accrementition of collagen fibers was obvious around the splenic corpuscle and central artery. The increased reticulate fibers encircled the splenic corpuscle with more connection between the fibers. The vascular endothelial cells were in diffused distribution, without any regionality in PH spleen, but the vessel with enlarged lumina increased in red pulp. Conclusions The morphological changes of the blood spleen barrier can be one of the pathological fundaments for the abnormality of the immune function and the increased destruction of blood cells located in the spleens of patients with PH However. this still entails clarification.     

基因芯片筛选门静脉高压症脾亢脾和正常脾巨噬细胞中差异表达基因

目的运用基因芯片技术检测门静脉高压症脾亢脾和正常脾巨噬细胞中基因表达的差异,探讨其在门静脉高压症脾亢发生中的意义。方法提取门静脉高压症脾亢脾巨噬细胞和正常脾巨噬细胞的总RNA,分别用标有荧光素的dCTP反转录制备cDNA探针,将探针与含有14112点cDNA的Biostar-H140scDNA表达谱芯片杂交后扫描荧光强度。上述方法重复3次,从而筛选出恒定的差异表达基因。结果3张芯片分别检测到896、1330和898个差异表达基因,恒定的差异表达基因共有121个,占总基因数的0.86%。其中表达上调的已知基因有21个,表达下调的已知基因有73个。差异表达基因涉及离子通道和运输蛋白、细胞周期蛋白类、细胞骨架和运动、细胞受体、细胞信号和传递蛋白、代谢、免疫相关等多个方面。这些基因可能与门静脉高压症脾亢的发病机制有关。结论采用基因芯片技术筛选门静脉高压症脾亢脾和正常脾巨噬细胞中差异表达的基因,可能为其病因和发病机制的研究提供新思路。     

部分脾动脉栓塞术治疗肝硬化门脉高压症46例

目的:探讨部分脾动脉栓塞术(PSE)治疗肝炎肝硬化门静脉高压症并发脾功能亢进的疗效及临床意义.方法:通过我院46例肝炎肝硬化门静脉高压症并发脾功能亢进患者行PSE,观察术前及术后血象变化、脾脏大小变化、门静脉内径变化及并发症情况.结果:与术前相比,术后白细胞及血小板计数明显上升,3 mo后稳定在一定水平,红细胞计数术前及术后无明显变化,脾脏3 mo后明显缩小,门静脉内径不同程度缩小,术后无严重并发症发生.结论:PSE治疗肝炎肝硬化门静脉高压症合并脾功能亢进安全有效.     

部分性脾栓塞治疗门静脉高压性脾功能亢进

对２１例门静脉高压脾功能亢进患者进行了部分性脾栓塞治疗。术后脾脏缩小、白细胞和血小板明显回升，凝血酶原时间缩短。结论：掌握好术前抗生素的使用、术中超选择的导管技术和合理的术后处理，栓塞量控制在术前脾脏体积的５０％～７５％之间，该方法具有栓塞效果肯定，安全及微创等特点。     

大鼠肝硬化形成过程中门静脉压力及血流动力学变化

目的:探讨大鼠肝硬化模型形成过程中门静脉压力及血流动力学的变化,建立有效的血流动力学特征研究模型. 方法: 选用雄性健康SD大鼠80只,随机分为4组,1组作为空白对照,其余3组建立大鼠肝硬化模型,分别于模型形成过程中第2,5,10 wk观察门静脉压力及血流动力学变化特点,并与前一组为对照进行比较. 结果: 试验组在注射四氯化碳(CCl4) 2 wk后门静脉压力明显升高为(10.23±0.36) mmHg (1 mmHg=0.133 kPa),并在10 wk内持续升高至(16.73±1.46) mmHg, 各组与其对照组相比有统计学意义(P＜0.01);门静脉内径、血流速度、血流量2 wk后即明显升高,分别为(0.185±0.015) cm, (13.30±0.96) cm/s, (12.40±2.95) mL/min,与对照组相比差异有统计学意义(P＜0.01),第5 wk流速(12.22±1.18 cm/s)与相应对照组比较有差异外,其余各项与相应对照相比差异均无统计学意义;充血分数注射后第2,5 wk与相应对照比较差异均有统计学意义(P＜0.01或P＜0.05). 结论: 在制备大鼠肝硬化模型过程中,第2 wk即可见明显血流动力学及压力改变,在第10 wk可形成稳定的大鼠肝硬化门脉高压症的血流动力学研究模型.     

肝硬化门脉高压患者肝动脉与门静脉病理变化分析

目的 研究肝硬化后门静脉高压病例大血管血管壁的组织结构改变,探讨诱导型一氧化氮合酶(iNOS)在肝硬化发生进程中的作用.方法 收集肝硬化肝移植病例的门静脉左支、左肝动脉和肝左静脉27例作为病例组,同期外伤性肝切除相应血管15例为对照组.分别予以HE染色、Masson染色,肝动脉加用弹力纤维染色和兔抗人 iNOS 多克隆抗体免疫组织化学. 结果 病例组门静脉内膜、中膜增厚,中膜平滑肌细胞增生、肥大,部分突出至内膜下;肝动脉内膜不规则增生,动脉管腔变窄,动脉壁内弹力膜变平、甚至断裂,中膜平滑肌向内膜增生;肝静脉壁组织结构没有明显改变.iNOS在肝动脉平滑肌细胞胞质呈高表达.结论 肝硬化患者肝动脉与门静脉血管壁会继发组织结构重建,这是人体自身代偿机制的结果,iNOS的高表达加速了该组织结构重建的发生、发展.     

A quantitative study on vascular angiotensin II receptors in rats with portal hypertension

Summary Angiotension-I (A-I) receptor maximal binding capacity (B_max) and dissociation constants (K_d) of different blood vessels in rats with prehepatic portal hypertension were studied by radioligand binding analysis. The results showed that the A-I receptor B_max in the thoracic aorta, superior mesenteric artery and portal vein of portal hypertensive animals (113. 7±19. 4 fmol/mg protein, 206. 9 ±39. 3 fmol/mg protein and 31. 5±9. 2 fmol/mg protein respectively) was all significantly lower than that of controls (146. 8±24. 5 fmol/mg protein, 297. 2±44. 7 fmol/mg protein and 53. 4±12. 1 fmol/mg protein respectively,P<0. 01). The A-I receptor K_d in the superior mesenteric artery was markedly increased in portal hypertensive animals (1. 03±0. 11 nmol/L) compared with that in controls (0. 88±0. 08 nmol/L,P<0. 05). In the thoracic aorta and portal vein, the A-I receptor K_d in portal hypertensive animals was slightly higher than that in controls, but no significant difference was observed between the two groups. The results suggested that the vascular hyporesponsiveness to A-I in portal hypertension was caused partially by a reduction in number and a decrease in affinity of vascular A-I receptors, and these changes might possibly lead to the formation of hyperdynamic circulation.     

丹参及其组分丹参酚酸B盐对门静脉高压小鼠肝脏微循环的影响

目的：研究活血化瘀中药丹参及其组分丹参酚酸B盐（salvianolic acid B,SA-B）对内皮素-1（endothelin-1,ET-1）所致门静脉高压（portalhypertension,PHT）模型小鼠肝脏微循环的影响。 方法：昆明种小鼠84只,随机分为模型组、内皮素A受体（endothelin A receptor,ETAR）阻断剂组、黄芪组、黄芪多糖组、延胡素组、丹参组、SA-B组,每组12只。预先灌胃等量药物或蒸馏水,1次／d,共3d。用微量注射泵以80μL／min速度从尾静脉注射ET-1（1．6μg／kg）,建立门静脉高压模型。每组中6只小鼠用激光多普勒测定尾静脉注射ET-1前后肝脏平均血流灌注量;另6只活体观察注射ET-1前后肝脏微循环流速。 结果：各组注射ET—1后肝脏平均血流灌注量均有不同程度的下降,但SA—B组和ETAR阻断剂组下降幅度较模型组小（P〈0．01）;黄芪组和黄芪多糖组下降幅度与模型组接近,与SA—B组比较,差异有统计学意义（P〈0．05）;SA—B组则与ETAR阻断剂组作用相当。从各组肝脏微血管流速的变化来看,SA—B组和ETAR阻断剂组流速下降幅度均小于模型组（P〈0．05,P〈0．01）;丹参组、SA—B组的下降幅度与ETAR阻断剂组相比,差异无统计学意义。 结论：丹参和SA-B能对抗ET-1引起的肝脏平均血流灌注量和微循环流速降低,这可能是其改善门静脉高压时肝脏微循环的机制之一。     

Treatment of portal hypertension from portal vein cavernoma with the meso-Rex bypass

Extrahepatic or prehepatic portal vein cavernoma and thrombosis is a more common condition in children than that in adult patients with extrahepatic or prehepatic portal vein obstruction (EHPVO),which involves approximately 30％ of children with portal hypertension and can involve all the portal hypertension complications.Cavernomatous transformation of the portal vein is common after portal thrombosis in non-cirrhotic patients.This challenging situation is relatively more frequent after liver transplantation,particularly in pediatric recipients.Acute bleeding from esophageal and gastric varices is temporarily treated by sclerotherapy or variceal banding.     

肝硬化门脉高压症患者手术90例麻醉管理

目的:探讨肝硬化门脉高压症患者手术麻醉管理的特点。方法:回顾分析90例肝硬化门脉高压症手术临床麻醉资料,其中上消化道大出血(失血性休克)急诊手术10例。采用气管内全麻45例,气管内全麻+连续硬膜外麻醉43例,连续硬膜外麻醉2例。结果:除1例术终广泛渗血,血压不稳,带气管导管回病房外,其余87例均于手术结束30 min内顺利拔除气管导管;术后一侧声带麻痹1例,保守治疗后声嘶症状消失;术终并发张力性气胸1例,立即行胸腔闭式引流;无椎管内麻醉并发症,全麻者无术中知晓发生。结论:肝硬化门脉高压症患者麻醉前应正确评估,合理选择麻醉方案,重视低蛋白血症和贫血程度,加强呼吸循环功能监测。     

肝脾固定治疗犬肝前性门脉高压效果观察

目的：通过动物实验验证肝脾固定治疗小儿肝前性门脉高压的可能性。方法：将犬随机分为实验组(n=10)和对照组(n=5),分别制造肝前性门脉高压模型,然后对照组关腹,实验组将肝脾加以固定后关腹,饲养12周后以彩超检查肝脾问血流情况,开腹测脾脏大小、门脉压力,抽取血样,经脾穿刺,行X线造影,并取活组织进行病理学检查。结果：2组动物模型的制作均获得成功,压力变化、病理结果、X线检查和彩超检查均证实实验组肝脾固定良好,能够将门脉血液分流回肝,降低门静脉压力。结论：肝脾固定后能有效降低门脉压力．治疗门脉高压具有可行性．并且更符合生理状态。     

Small-diameter prosthetic H-graft portacaval shunts in the treatment of portal hypertension

Background Portasystemic shunts, especially total shunts, are effective tools for reducing portal pressure and controlling variceal bleeding but lead to high risk of encephalopathy and accelerating liver failure. The purpose of this study is to evaluate the clinical effects of small-diameter expanded polytetrafluoroethylene (ePTFE ) H-graft portacaval shunts in the treatment of portal hypertension.Methods Thirty-one patients with portal hypertension were treated with ePTFE small-diameter H-graft portacaval shunts from December 1995 to April 2002. Twenty-one had externally ringed grafts and 10 had non-ringed grafts; 20 had 10 mm diameter grafts and 11 had 8 mm grafts. The left gastric artery and coronary vein were ligated in 22 patients. Additionally, 6 patients underwent pericardial devascularization, and splenectomies were performed on 30 patients.Results An average decrease of free portal pressure (FPP) from (32. 13 ±4. 86) cmH2O before shunting to (12. 55 ±5. 57) cmH2O after shunting was observed.     

合并胆囊结石的肝硬化门脉高压症的治疗

目的探讨合并胆囊结石的门脉高压症合理的治疗方法。方法分析总结我院2002年-2009年收治的34例合井胆囊结石的门脉高压症患者的临床资料。结果5例行断流术,22例一期联合断流及胆囊切除术,7例断流术后2期胆囊切除。34倒中1例死亡,有7例发生9种近期并发症,经治疗痊愈。结论合并胆囊结石的肝硬化门脉高压症一期化断流联合胆囊切除手术安全有效。     

选择性断流术治疗门静脉高压症的临床研究

目的 研究选择性断流术对门静脉高压症临床疗效及转归的影响.方法 回顾性分析1994年1月至2006年12月收治的门静脉高压症患者187例的临床资料,分为保留食管旁静脉组(选择组)154例和未保留食管旁静脉组(传统组)33例.通过对临床疗效的观察、术中自由门静脉压(FPP)的动态监测、术后肝功能变化的检测以及术后近期并发症的发生情况进行对比研究.结果 术后两组患者FPP均下降,与术前比较差异有统计学意义(P＜0.01),且选择组FPP降幅大于传统组(P＜0.01);术后选择组近期并发症总发生率和死亡率均明显低于传统组(P＜0.01);术后1周选择组天冬氨酸氨基转移酶(AST)明显降低,与术前比较差异有统计学意义(P＜0.01),其余肝功能指标与术前比较差异无统计学意义(P＞0.05).结论 选择性断流术能更有效地降低门静脉压力,确切控制食管及胃底部曲张静脉破裂出血,降低术后近期并发症的发生率,并有利于肝脏功能的恢复.     

Effects of hepatotrophic factors on the liver after portacaval shunt in rats with portal hypertension

Background Portacaval shunt （PCS） prevent hepatotrophic factors from flowing into the liver, but they enter directly the systemic circulation and worsen liver injury. This study was designed to investigate the effects of hepatotrophic factors through the portal vein on the liver in rats with portal hypertension after portacaval shunt. Methods Intrahepatic portal hypertension （IHPH） was induced by intragastric administration of carbon tetrachloride, and end-to-side PCS was performed. Eight normal rats served as controls, and eight rats with IHPH served as IHPH model （IHPH group）. Another 32 rats with IHPH-PCS were randomly subdivided into 4 groups： normal saline （NS） given to 8 rats, hepatocyte growth factor （HGF） 8, insulin （INS） 8, hepatocyte growth factor and insulin （HGF＋INS） 8. Hepatotrophic factors were infused into the portal vein through an intravenous catheter. Portal venous pressure （PVP） was measured. The levels of serum alanine aminotransferase （ALT） and aspartate aminotransferase （AST） were tested biochemically and those of hyaluronic acid （HA） and laminin （LN） were measured by radioimmunoassay. Hepatic fibrosis was assessed histologically and the expression of collagens type I and In were detected immunohistochemically. Ultrastructural change of hepatocytes and the number of mitochondria were observed under an electron microscope. The data were compared between groups and subgroups by Student-Newman-Keuls procedure with SPSS 10.0. Results PVP was significantly higher in the IHPH rats than in the control rats （P〈0.05）. The levels of serum ALT, AST, HA, and LN, hepatic fibrosis score, the amount of collagen deposition, collagens type I and III increased more significantly in the IHPH group than in the control rats （P〈0.05）. The number of mitochondria decreased more significantly in the IHPH rats than in the control rats （P〈0.05）. The levels of serum ALT, AST, HA and LN as well as hepatic fibrosis score, the amount of collagen deposition, and the amount of collagens type I and M in the HGF and HGF＋INS rats were significantly lower than those in the NS rats （P〈0.05）. The damage to hepatocyte ultrastructure was markedly alleviated and the number of mitochondria was increased more significantly in the HGF and HGF＋INS rats than in the NS rats under an electron microscope. Conclusions Perfusion of exogenous hepatotrophic factors through the portal vein can alleviate liver injury, minimize the damage to the ultrastructure of hepatocyte, protect liver function, and lessen hepatic fibrosis in rats with portal hypertension after PCS.     

原发性肝癌合并门静脉高压症的手术选择

目的:探讨原发性肝癌合并门静脉高压症的手术方法及疗效.方法:回顾分析手术治疗原发性肝癌合并门静脉高压症120例资料.结果:手术并发症和手术病死率分别是18.5%和5.6%.术后1,3,5,7年生存率分别是79.5%,40.6%,35.2%,9.3%.结论:个体化治疗原则是提高原发性肝癌合并门静脉高压症治疗效果的关键.     

Management of gastric cancer in patients with sinistral portal hypertension

Sinistral portal hypertension (SPH) is usually caused by pancreatic pathology and is characterized by splenic vein thrombosis with or without portal vein thrombosis.1 The increased pressure caused by splenic vein occlusion is transmitted via the short gastric and gastroepiploic veins to the portal system.The reversal of blood flow in the left gastric vein results in gastric varices.In patients with SPH,especially those with occlusion of both the splenic and portal veins,the main or even the only pathway of splenic venous return to the portal vein is via the gastric varices,and these patients require special management during gastric surgery.     

缬沙坦抗大鼠肝纤维化及降低门静脉高压的实验研究

目的探讨缬沙坦降低大鼠肝硬化门静脉高压的疗效及作用机制。方法采用复合因素制造肝硬化门静脉高压模型,成模后将大鼠分为缬沙坦组、模型组,另设正常对照组。分别给予缬沙坦及等量的蒸馏水灌胃,治疗15d,各组于治疗结束测门静脉压力(PVP)、平均动脉压(MAP)、心率(HR),肝功能,血清透明质酸(HA)、Ⅲ型前胶原(PCⅢ),肝脏组织学,免疫组织化学染色法检测肝脏α-平滑肌肌动蛋白(α-SMA)的表达。结果与模型组比较,缬沙坦组PVP明显降低[分别为(9.2±1.7)mmHg和(13.3±2.3)mmHg,P<0.01];MAP和HR无明显变化[分别为(80.7±28.9)mmHg比(88.5±11.8)mmHg,(367±56)次/min比(381±51)次/min,P>0.05],同时HA、PCⅢ和α-SMA表达水平也较模型组降低[分别为(409.70±196.41)ng/ml比(723.71±121.41)ng/ml,(82.69±20.06)μg/L比(118.73±31.81)μg/L,(0.27±0.09)%比(2.26±0.34)%,P<0.01]。结论缬沙坦可安全、有效地降低大鼠肝硬化门静脉压力,可能与作用于肝星状细胞有关,有良好的应用前景。     

血管紧张素Ⅱ受体阻滞剂治疗肝硬化门脉高压的研究

目的通过与非选择性β-受体阻滞剂普奈洛尔的比较探讨血管紧张素Ⅱ受体阻滞剂洛沙坦对肝硬化门脉高压病人门静脉压力的影响.方法选择肝硬化伴门脉高压患者32例,随机分为洛沙坦(25 mg/d)治疗组和普奈洛尔(30～80 mg/d)治疗组,在治疗前和治疗2、3周时分别应用彩色多普勒超声仪测量每位患者的门静脉内径(DPV)及门静脉血流速度(VPV),对比这两种药物对门静脉压力影响.结果普奈洛尔组治疗后DPV下降、VPV增快,治疗前后的数值分别为,(14.44±1.41)mm,(7.75±1.20)cm/s及(12.13±1.49)mm,(11.25±1.82)cm/s,P＜0.05.洛沙坦组治疗后DPV亦明显下降,VPV增快,治疗前后数值分别为,(14.69±1.31mm,7.50±1.22)cm/s及(12.00±1.37)m,(11.00±1.54)cm/s,P＜0.05.但两组药物之间无统计学差异.在笔者的研究过程中,这两组患者均未发生有意义的不良反应.结论血管紧张素Ⅱ受体阻滞剂洛沙坦和非选择性β受体阻滞剂普奈洛尔一样,是一种安全、有效的降低肝硬化门脉高压患者门静脉压力的药物.     

心得安对门静脉高压患者自由门静脉压的影响

目的探讨心得安对肝硬化并发门静脉高压患者降低自由门静脉压的效果。方法56倒门静脉高压患者，按比lchild肝功能分级方法，分为A级（18例）、B级（30例）、C级（8例）三组。在术中于断流前与用药前和静注心得安(5mg）30min后，分别测定自由门静脉压（FPP）.统计学处理采用t检验。结果全组病人在应用心得安后，FPP均有明显下降，按肝功能Child分级法，A、B‘C三级用药前比较，分别为P＜0、001、P＜0、001和尸＜0、02。结论心得安可以降低门静脉高压症患者的自由门静脉压，因而可防治多数门静脉高压患者由静脉曲张导致的上消化道再出血。