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。     

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。     

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。     

哮喘模型大鼠气管的张开角及残余应变

对哮喘模型大鼠气管的无载荷状态和零应力状态进行分析。与正常组相比，模型大鼠气管软骨剪开的张开角及所对应的残余应变绝对值均较正常组显著增大（P〈0．05），而且随着x／L的增大而呈明显上升趋势。模型大鼠气管肌肉剪开的张开角及所对应的残余应变绝对值无显著变化，且沿气管轴向变化不明显。结果表明哮喘大鼠气管为了适应外在应力环境的变化，肌肉部分不断进行代偿性生长，导致哮喘大鼠气道重建。     

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.     

大鼠气管的零应力状态

大鼠气管存在残余应力,将无载荷状态的气管环径向剪开,气管环展开成扇形体,即得到气管的零应力状态。文章结果表明,对于大鼠无载荷状态气管环,软骨剪开与肌肉剪开所展成的张开角是不同的,软骨剪开对应的张开角明显大于肌肉剪开的张开角。而且肌肉剪开的张开角沿气管轴向变化不明显,而软骨剪开的张开角随着ｘ／Ｌ的增大而呈明显上升趋势。本文结果对分析气管在特定力学环境中的适应性生长是有帮助的。     

大鼠气管的周向残余应变及其非均匀分布

本文对大鼠气管的无载荷状态和零应力状态进行分析，发现肌肉剪开无载荷气管环所对应张开角较小，而且基本上不随气管轴向位置变化；与此不同，软骨剪开无载荷气管环所对应张开角较大，而且随气管轴向距离的增大有明显的上升趋势。结果表明，无载荷气管存在残余应变，内壁为压缩应变，外壁为拉伸应变，残余应变与气管张开角之间呈正相关的定量关系。本文所得结果对深入认识气管零应力状态，研究气管为适应所处力学环境产生的气管重建是十分必要的。     

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。     

血流切应力变化导致颈总动脉重建及其对血管平滑肌细胞凋亡和分化的影响

目的　探讨动脉血流切应力变化对动脉壁形态结构、零应力状态以及血管平滑肌细胞(vascular smooth muscle cells，VSMC)凋亡和去分化的影响。方法　结扎大鼠左侧颈总动脉的部分分支，使血液全部经由枕动脉流出，造成左颈总动脉(LCA)低血流和低切应力以及对侧右颈总动脉(RCA)高血流和高切应力状态，以假手术不结扎动脉的动物为正常对照。取LCA和RCA，光镜和透射电镜观察血管壁组织形态学变化；测量血管零应力状态下的张开角；TUNNEL法进行原位细胞凋亡检测；免疫印迹法检测VSMC表型分化标志分子hl-calponin的表达。结果　术后7d，低切应力LCA的内径减小了13%左右，壁厚内径比显著增加，张开角显著减小；内皮下层明显增厚，VSMC凋亡数量显著增加，VSMC表型分化标志分子hl-calponin的表达量显著降低。结论　血流切应力显著降低会在短期内引起血管重建，提示VSMC凋亡和去分化可能是低血流和低切应力导致血管重建的早期事件之一。     

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。     

Statistical Characterization of Portal Images and Noise from Portal Imaging Systems

In this paper, we consider the statistical characteristics of the so-called portal images, which are acquired prior to the radiotherapy treatment, as well as the noise that present the portal imaging systems, in order to analyze whether the well-known noise and image features in other image modalities, such as natural image, can be found in the portal imaging modality. The study is carried out in the spatial image domain, in the Fourier domain, and finally in the wavelet domain. The probability density of the noise in the spatial image domain, the power spectral densities of the image and noise, and the marginal, joint, and conditional statistical distributions of the wavelet coefficients are estimated. Moreover, the statistical dependencies between noise and signal are investigated. The obtained results are compared with practical and useful references, like the characteristics of the natural image and the white noise. Finally, we discuss the implication of the results obtained in several noise reduction methods that operate in the wavelet domain.     

Portal tract fibrogenesis in the liver

The portal area is the 'main entrance' and one of the two main exits of the liver lobule. Through the main entrance portal and arterial blood reach the liver sinusoids. Through the exit the bile flows towards the duodenum. The three main structures, portal vein and artery with their own wall (and vascular smooth muscle cells) and bile duct with its basal membrane, are surrounded by loose myofibroblasts and by the first layer of hepatocytes and non-parenchymal cells. Chronic diseases of the liver can lead to development of liver cirrhosis, characterized by formation of fibrotic septa which can be portal-portal in the case of the chronic biliary damage or portal-central in the case of the chronic viral hepatitis. Central-central septa can also be observed under other pathological conditions. When damaging noxae are introduced to the liver, inflammatory cells are first recruited to the portal field, the first layer of hepatocytes may be destroyed (enlargement of the portal field) and portal (myo)fibroblasts become activated. A similar reaction may take place when the target of inflammation is the bile duct with consecutive reduction of the bile flow, activation of the portal (myo)fibroblasts, proliferation of bile ducts and destruction of the hepatocytes around the portal field. Increased matrix deposition may be the consequence. During the past years several publications dealt with the pathomechanisms of portal fibrogenesis as well as with its resolution. One of the most intriguing observations was that it is not hepatic stellate cells of the hepatic sinusoid, but portal (myo)fibroblasts which rapidly acquire the phenotype of 'activated' (myo)fibroblasts in the early stages of cholestatic fibrosis. These may also become the main mesenchymal cells of the porto-portal or porto-central fibrotic septa. This article reviews the similarities as well as differences between the mesenchymal cells of the portal tract and of the fibrotic septa vs 'activated' stellate cells of the hepatic sinusoids, and discusses the debate over their relative contributions to liver fibrogenesis.     

多层螺旋CT门静脉成像在评估肝硬化门脉侧枝血管中的价值

目的:评价多层螺旋CT门静脉成像显示门静脉高压的价值.材料与方法:30例门脉高压患者进行了螺旋CT门脉成像检查,其中10例患者又进行了门静脉造影检查(间接法).30例患者中全部存在侧枝循环,多数病例有2个或2个以上部位侧枝循环.结果:多层螺旋CT门静脉成像不仅显示了肝内门静脉2～3级分支,还显示了整套门脉侧枝血管系统.在三维门脉像上,脾门静脉曲张29例(占96.7%),其中1例脾静脉因栓子部分闭塞而狭窄,另有1例则完全栓塞血管未显示.胃左静脉曲张28例(占93%),食管或食管旁静脉曲张27例(占90%),胃短静脉(胃后静脉)曲张19例(占63%),胃肾分流血管10例(占33%),腹膜后静脉曲张9例(占30%),脐周静脉曲张伴腹壁静脉曲张6例(占20%).10例患者CT三维门脉像与间接门静脉造影作比较,前者对门静脉及其侧枝循环的显示好于后者.结论:多层螺旋CT门脉成像是门静脉无创性检查的可靠方法,有较高的临床运用价值.