门静脉高压症经颈静脉肝内门体分流术(TIPS)血液动力学分析

经颈静脉肝内门体分流术（TIPS）是治疗门静脉高压症的有效手术之一。本文提出了一个集中参数模型对TIPS进行血液动力学分析。首先根据门脉高压的前向血流学说和后向血流学说，计算了门静脉系统血液动力学参数，然后计算了TIPS术后门静脉系统血液动力学参数的变化，并详细分析讨论了这些血液动力学参数随肝硬变梗阻程度的变化，以及TIPS分流道阻力对它们的影响。结果表明所得结果和临床所测参数吻合较好，该模型可进一步应用于门脉高压症和其它分流术血液动力学机理研究，并为临床应用提供参考。     

肝前型门静脉高压兔门脉系统血管应力的研究

门脉高压症是肝硬化常见的病理生理改变.本研究采用两步门静脉结扎法制备门脉高压症(PHT)兔模型;检测不同时间点门静脉及小肠系膜曲张静脉的直径,不同程度曲张静脉及门静脉主干的血流动力学和应力(压力、剪应力和周向应力)大小.随着小肠系膜曲张静脉直径的增大,PHT兔门脉与小肠系膜静脉压力显著增加,剪应力减小,周向应力增大;两部位间应力(压力、剪应力和周向应力)呈直线正相关.研究表明,门脉高压时门脉系统处于低剪应力与高周向应力状态,这可能是门脉高压症并发症发生的力学基础.     

实验性肝硬化的病理变化形成过程中门静脉血流动力学的改变

目的:通过对实验性大鼠肝硬化时门静脉血流动力学的变化,了解门脉高压的形成过程。方法:健康Wistar大鼠皮下注射四氯化碳,观察肝组织的病理改变过程中其门静脉血流动力学的变化。结果:实验性肝硬化过程中肝细胞经历变性、坏死、纤维组织增生及假小叶的形成。门静脉内径、血流速度、流量在注射四氯化碳2周后明显升高(P＜0.05或P＜0.01);15周时由于形成了侧枝循环,上述测值又明显低了(P＜0.01);注射四氯化碳大鼠门脉充血分数除在10周时变化无统计学意义外(P>0.05),2周、5周、15周时均比前一组明显高(P＜0.05或P＜0.01)。结论:大鼠在肝硬化形成过程中门静脉血流动力学变化与肝组织的病理改变均发生了变化。     

“肝脏反馈机制”并非门脉高压症高动力循环的发生机制

观察“肝脏反馈机制”在门脉高压症（ＰＨＴ）内脏高动力循环发生过程中的作用，检测了门静脉分支结扎（ＰＢＬ）大鼠和门静脉缩窄肝前型ＰＨＴ（ＰＶＬ）大鼠不同时期的血流动力学变化。结果显示：ＰＢＬ术后７天由于门静脉阻力增加，门静脉压力出现一过性增高，第５，７天出现类似于ＰＶＬ大鼠的短暂的全身高动力循环状态，整个实验过程中，尽管ＰＢＬ大鼠部分肝脏失去了门静脉血供，但未发现象ＰＶＬ大鼠所表现的内脏血管阻力下降     

胃与食管静脉的临床解剖学

随着内窥镜广泛应用于临床,许多作者报告,在部份门脉高压上消化道大出血的病人中,不是由食管静脉曲张破裂出血所致,而是来自急性胃粘膜损害,由门脉高压引起的急性胃粘膜损害,亦称“门脉高压性胃炎”PortalHypertensive Gastritis简称PHG。近几年来,国内、外有些临床医帅主张对食管静脉曲张采用硬化剂注射疗法,由于阻断了胃左静脉→食管静脉→奇静脉间的侧枝循环径路,可导致异位静脉曲张的形成和破裂出血,临床上将食管、胃底以外的曲张静脉统称之为“异位静脉曲张”Ectopic Varices简称EV。熟悉胃和食管的血液供应情况,特别是静     

大鼠肝内型门脉高压症形成中门静脉力学性质的变化

目的观察大鼠肝内型门脉高压症形成中门静脉零应力状态及轴向拉伸时张应力．伸长比关系的动态变化，探讨门静脉生物力学特性的变化在门脉高压症形成中的作用。方法以60％四氯化碳(CCl4)皮下注射法制备肝内型门脉高压症大鼠模型，采用生物力学技术测定CCl4注射第2、4、6、8、10周大鼠门静脉零应力状态张开角和轴向拉伸时张应力，伸长比关系，并同步监测大鼠门静脉压力(PVP)、门静脉流量(PVF)、平均动脉压(MAP)、门静脉阻力(PVR)和内脏血管阻力(SVR)等血液动力学指标的动态变化。结果随着CCl4注射时间的延长，实验组大鼠的血液动力学指标发生了显著的变化。与之相对应．大鼠门静脉张开角及轴向拉伸参数b亦逐渐增大，从注射第10周起与对照组相比具有统计学差异(P＜0．05)。结论门脉高压症大鼠存在高动力循环状态(HCS)。HCS可引起门静脉血管生物力学特性的变化。     

门脉注射聚氨酯-四氢呋喃溶液制备犬门脉高压症模型

介绍一种利用聚氨酯高分子材料和有机溶剂四氢呋喃配制的溶液制备犬门脉高压症动物模型的方法,并评价成模效果。选用西安本地杂种犬12只,取上腹部小切口,经门静脉推注8%(W/V)的聚氨酯-四氢呋喃溶液建立门脉高压症模型。分别在造模前、造模中、造模后4、8、12周测量实验犬门静脉压力,以造模前门静脉压力作为正常参考值,评估模型建立效果。结果显示经门静脉注射聚氨酯-四氢呋喃溶液后门静脉压力可立即升至造模前的2.5倍,4周后门静脉压力维持在造模前的1.5倍以上。该法制备犬门脉高压症模型操作简单、死亡率低、门静脉压力维持稳定,尤其是腹腔粘连极轻,门静脉的结构和位置保持正常,非常适合外科手术治疗门脉高压症方面的研究。     

门脉高压症患者术前术后的观察与护理

门脉高压症是因门静脉血流受阻。血液淤滞,如肝硬化、血栓和肿瘤引起门静脉系统压力增高的一种病理状态,主要表现有脾肿大、脾机能亢进。食管、胃底静脉曲张并发破裂引起上消化道大量出血是门脉高压症致命的并发症,其死亡率在30％以上。因此,急性大出血经非手术治疗48h无效即应紧急手术     

大鼠肝前性门静脉高压症形成中一氧化氮和内皮素-1水平的动态变化

目的:观察大鼠肝前性门静脉高压症形成中一氧化氮(NO)和内皮素-1(ET-1)水平的动态变化,探讨其在门静脉高压症高动力循环中的作用。方法:以部分门静脉结扎(PVL)法复制肝前性门静脉高压症大鼠模型,分别用硝酸还原酶和放免法检测正常组、假手术(SO)组及PVL组术后不同时点的门静脉血浆NO^-₂/NO^-₃、ET-1水平,并同步监测血流动力学指标的动态变化。结果:PVL术后各时点NO^-₂/NO^-₃水平显著高于而ET-1水平显著低于正常组,同时伴有血流动力学的明显变化。结论:门静脉高压症大鼠存在高动力循环状态(HCS)。NO和ET-1参与HCS的形成和维持。     

彩色多普勒超声观测TIPSS术前后门脉血流动力学变化

彩色多普勒超声观测ＴＩＰＳＳ术前后门脉血流动力学变化为探讨ＴＩＰＳＳ术后门脉血流动力学变化，及彩色多普勒超声对评价疗效的应用价值。采用彩色多普勒超声观察了３２例肝硬化门脉高压症患者门脉血流方向，并测量门静脉、脾静脉和内支架的血流速度。３２例患者３１例...     

Autoregulation of portal circulation: A correlative study of circulation and vascular morphology

To Investigate the mechanism of portal circulation and the genesis of portal hypertension, an in vivo model was made to Increase portal venous flow (PVF) by forming a bypass shunt between the femoral artery to the spienic venous branch in pigs and dogs via a regulatable pump. Using this model, an autoregulatory hemodynamics of the portal circulation and corresponding morphological changes of the intrahepatic vascular system were determined. Immediately after blood flow increase (100 mL/min) to the portal vein, PVF increased to the baseline level plus bypass shunt flow. But, PVF returned to the baseline level within 1 h for both animals. Portal venous resistance (PVR) at 1 h was significantly higher than the baseline level (R0.05). By histometric analysis of the cross-sectional area of the portal and hepatic venous branches (CSA-PV, CSA-HV) using the biopslzed liver, CSA-HV at 1 h was 27.6% of the CSA-HV of the baseline level in dog, which showed narrowing and contractive changes of the hepatic venous branches, and CSA-PV at 1 h was 36.4% of the CSA-PV of the baseline level In pig. which showed narrowing and contractive changes of the portal venous branches. It Is suggested that a tone of the intrahepatic vascular system has an important role In the portal autoregulatory hemodynamics.     

Gastric mucosa in patients with portal hypertension: prevalence of capillary dilatation and Campylobacter pylori.

To determine whether the "congestive" gastropathy associated with portal hypertension showed distinctive histological features independent of inflammatory gastritis, endoscopic biopsy specimens of gastric mucosa from 23 patients with portal hypertension and 25 patients with non-ulcer dyspepsia were examined. Active chronic gastritis associated with Campylobacter pylori was found in three patients with portal hypertension compared with 13 patients with non-ulcer dyspepsia. The changes of reflux gastritis were seen in nine patients with portal hypertension compared with three patients with non-ulcer dyspepsia. Mucosal capillary dilatation, assessed on sections stained for factor VIII related antigen, a specific marker for endothelial cells, was significantly greater in biopsy specimens from patients with portal hypertension but this difference was not apparent on sections stained conventionally. The degree of capillary dilatation was unrelated to the presence of histological gastritis. These observations support the view that portal hypertension is associated with a distinctive gastropathy characterised by prominence and dilatation of mucosal capillaries.     

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.     

Fibrous thickening of the splenic capsule. A response to chronic splenic congestion

Fibrous thickening of the splenic capsule is often seen in patients with hepatic cirrhosis or portal hypertension from other causes. However, most cases of capsular thickening have been considered idiopathic, with no obvious abnormality of the portal circulation. The possibility that these "idiopathic" cases also have evidence of portal hypertension was examined in a retrospective study. The splenic capsule thickness was measured in 434 consecutive autopsy specimens. Various clinical and autopsy parameters relevant to vascular disease were recorded and correlated with splenic capsular thickness. Thickened capsules were significantly more frequent in patients with advanced age, clinical history of severe congestive heart failure, cirrhosis, and hepatic portal sclerosis. It is suggested that most cases of splenic capsular thickening are caused by splenic congestion with organization of capsular and subcapsular hemorrhages.     

Intrahepatic portal vein sclerosis in patients without a history of liver disease. An autopsy study.

Portal fibrosis with portal venous obliteration is characteristic of noncirrhotic portal hypertension, but similar lesions are also commonly seen in patients without clinical evidence of liver disease. Thus, the ability to predict the presence of portal hypertension with histologic criteria will probably depend on a quantitative assessment of liver tissue. The purpose of this study is to provide a quantitative basis in a "normal" population for evaluation of portal vein obliteration. We reviewed 414 consecutive autopsies of patients without known history of alcoholism or clinical liver disease. Intrahepatic portal vein obliteration was graded 0 to III. The grading system was standardized by morphometry on 34 selected cases. The incidence of portal vein lesions increased with age and reached a plateau at about 60 years of age. Lesions were more common in patients who had severe congestive heart failure or arterial thrombosis. These associations suggest that obliterative lesions may be the result of thrombosis in patients with sluggish portal blood flow or hypercoagulability. Portal tract mineral oil deposits may also have a role, because they were found more often than expected in livers with portal sclerosis.     

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。     

Metoprolol in portal hypertension

Summary In a controlled trial, the effect of the ₁-selective blocking agent metoprolol on cirrhotic portal hypertension was investigated. A sustained reduction of portal pressure was observed in 60% of the treated patients after 1 and 2 months. No correlation between changes of portal pressure and cardiac output was established. This may indicate a direct action of-blocking substances on the splanchnic vascular system. The results suggest that treatment with metoprolol may be of value in patients with portal hypertension secondary to cirrhosis of the liver. However, to eliminate nonresponders the pressure has to be measured repeatedly.     

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。