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     

“化学性胆囊切除术”的实验研究

为研究胆囊化学切除硬化剂及可行性,将32只兔分4组(n=8)。剖腹直视下金属夹/丝线阻断胆囊管,底部造口注入硬化剂。1组:95%乙醇 5M三氟醋酸(TFA);2组:95%乙醇 2MTFA;3组:95%乙醇 1M TFA;4组:生理盐水(对照)。2、4、8周分批处死动物,胆囊作大体、光镜、透射电镜观察。结果:2周胆囊粘膜脱落坏死,4~8周纤维疤痕化。1、2组纤维化成功率高于3组,有显著性差异(1、2组∞3组:P<0.05),1、2组之间无显著性差异(P>0.05)。1组见肝细胞损害,3组有粘膜上皮再生。血管夹与丝线对致纤维化率无差异(P>0.05)。结论:胆囊硬化治疗后4~8周形成纤维疤痕,95%乙醇 2M TFA效果最佳,金属夹能阻断胆囊管。     

一期门静脉缩窄法复制大鼠门静脉高压性胃病模型

目的　复制周期短 ,操作简便的门静脉高压性胃病 (PHG)模型。方法　Wistar大鼠 72只 ,一期门静脉缩窄法 (PVL)缩窄门静脉横截面积 90 %制备模型 ,双色素造影直接观察大鼠术后不同时间胃壁动静脉短路 (A V短路 )开放情况并作定量计数。结果　大鼠术后单位面积A V短路计数PVL第 1天从 (11.2 8± 0 .34 )个 /cm2 增加到 (33.14± 0 .5 2 )个 /cm2 ,差异有非常显著性 (P <0 .0 1) ,第 15天达最高峰 (42 .2 0± 0 .86 )个 /cm2 。A V短路与门静脉压呈正相关 (r =0 .86 ,P <0 .0 1)。结论　PVL大鼠是目前PHG研究的较合适模型。     

放射性微球技术在门脉高压症研究中的应用

放射性微球技术在门脉高压症研究中的应用管洪庚综述陈易人审校（苏州医学院附属第一医院普外科２１５００６）应用血管内放射性微球技术（ｉｎｔｒａｖａｓｃｕｌａｒｒａｄｉｏａｃｔｉｖｅｍｉｃｒｏｓｐｈｒｅｔｅｃｈｎｉｑｕｅＲＭＴ）检测器官或组织内血流量，其准...     

胰源性区域性门脉高压症临床诊治

目的探讨胰源性区域性门脉高压症的诊断和治疗方法。方法回顾分析我院10年来共21例胰源性门脉高压的诊断和治疗措施及结果和随访。结果5例胰腺癌患者死于原发病复发转移,1例合并门脉血栓患者死于肠坏死,余无再出血。结论对于胰源性区域性门脉高压症,胰腺病史和胃镜、超声内镜及血管造影等检查发现胃底静脉曲张结合脾肿大及肝功能正常可协助明确诊断。胰源性门脉高压症可以通过脾切除术或同时结合贲门周围血管离断术治愈,但需结合原发胰腺疾病的治疗。     

阻断4-BB/4-1BB配体信号通路对抑制大鼠肝脏移植免疫排斥反应的实验研究

Background Blocking the 4-1BB/4-1BB ligand （4-1BBL） signal may modulate the secretion of Th1/Th2 cytokines and prolong the survival of the grafts, which play a key role in organ transplantation tolerance. The aim of this study was to investigate the role of blockade of the 4-1BB/4-1BBL co-stimulatory pathway with 4-1BBL monoclonal antibody （mAB） in acute rejection of rat orthotopic liver transplantation. Methods The orthotopic liver transplantation model was set up, while male Lewis rats were used as liver donors and Brown-Norway rats as recipients. The recipient rats were intravenously injected with anti 4-1BBL mAB or isotype control antibody. Groups were monitored for graft survival after transplantation. Plasma chemistry, including aspartate transaminase （AST）, alanine aminotransferase （ALT）, and bilirubin （BIL）, was assayed. The concentrations of interleukin （IL）-2, IL-10 and interferon （IFN）-γ in plasma were also measured by enzyme-linked immunosorbent assay. Allograft histology images were collected under light microscope and electron microscope. Results Isotype antibody treated recipients exhibited elevated plasma levels of liver injury markers including AST, ALT and BIL, progressive portal and venous inflammation and cellular infiltration of the liver ailografts, and a mean graft survival time （MST） of 10.9 days. Administration of anti 4-1BBL mAB resulted in a decrease in plasma levels of liver injury markers and the concentrations of IL-2, IL-10 and IFN-γ. The histological grade of rejection on day 7 decreased and MST （17.3 days） increased substantially. Conclusions These results demonstrate that attenuation of acute rejection follows the blockade of the 4-1BB/4-1BBL co-stimulatory pathway with 4-1BBL monoclonal antibody and strongly suggest it is a promising strategy to prevent progression of graft rejection by suppressing T cell-mediated immunity.