20%小体积的大鼠肝脏移植模型

目的 应用显微外科技术建立20%小体积移植物的大鼠原位肝脏移植模型.方法 原位移植建立20%小体积大鼠肝脏移植模型.雄性Lewis大鼠40只,供体20只,受体20只.供肝经门静脉用4℃ UW液灌注.肝上下腔静脉用端端吻合连续缝合的方法.肝下下腔静脉和门静脉分别用套管方法固定.套叠缝合法重建肝动脉.胆管重建采用内支架管端端连接的方法.观察移植物的存活率.免疫组化检测肝细胞摄取溴脱氧尿核苷的情况.结果 共施行肝脏移植手术20例,移植手术成功率为100%.20%小体积肝脏移植物的存活率为93.8%(＞14 d).组织学检查移植后的肝脏组织结构良好.移植术后72 h溴脱氧尿核苷染色阳性的肝细胞计数明显增多.结论 20%小体积大鼠肝脏移植物可启动完成移植后的肝脏再生.显微外科技术是移植模型成功的关键.该模型稳定性强,适合于部分肝脏移植领域的基础研究.     

小鼠50%体积肝脏原位移植实验模型的建立

目的 介绍一种小鼠50%体积的原位肝脏移植实验模型.方法 选择同系雄性C57BL/6小鼠,供、受体各28只.实验分为50%体积移植组和全肝移植对照组.50%肝脏移植物通过切除左侧肝叶获得.供肝经门静脉灌注4℃威斯康星大学保存液.血管重建时,肝上腔静脉端端吻合,门静脉和肝下腔静脉采用袖套法吻合.不作动脉重建.术后观察移植物的存活时间.组织病理学检查肝脏移植物的组织结构和细胞形态,免疫组化检测肝细胞复制情况.结果 小鼠肝脏移植手术成功率为100%.50%体积的小鼠肝脏移植受体存活率为90%(＞15 d).全肝移植受体存活率为100%(＞15 d).所有受体手术无肝期保持在23 min内.术后组织学检查移植肝组织结构良好,全肝移植后肝脏再生反应不明显.50%体积的肝脏移植后激发明显的再生反应.结论 小鼠50%体积的肝脏移植实验模型存活率高,术后激发明显的再生反应.该模型可应用于缺血再灌注损伤和肝脏再生等基础研究.     

日本ABO不相容活体供肝肝脏移植现状

通常认为ABO不相容活体供肝肝脏移植可能会由于抗体介导排斥(antibody-mediated rejection,AMR)导致移植物失功,但是随着近年来各种技术及方法的改善,日本进行了部分ABO不相容活体供肝肝脏移植以缓解器官短缺的矛盾,疗效有明显提高,     

自体脾移植及食管横断吻合术后门静脉高压症患者肝脏形态学改变的MR研究

目的探讨自体脾移植及食管横断吻合术对肝硬化门静脉高压症（PHT）患者肝脏形态学改变的影响。方法将40例PHT患者随机分为研究组和对照组,各20例,均进行食管横断吻合术,对照组做全脾切除,研究组脾部分腹膜后移植。手术前后用磁共振（MR）测量肝体积及形态学的变化。结果术前研究组肝体积为（1054．06±289．66）cm3,对照组为（1108．72±253．84）cm3,两组肝体积差异无统计学意义。手术后研究组肝体积为（1063．74±193．13）cm3,对照组为（1092．25±206．44）cm3,两组肝体积差异无统计学意义。MR检查手术前后肝脏表面、肝裂、肝实质细网状或粗网状结构显像无差异,但与对照组相比,研究组术后肝内结节影像有所改善（P〈0．05）。结论自体脾移植及食管横断吻合术没有促进肝纤维化的进展。     

不同体积肝脏移植疗效的实验研究

我们拟通过体外减体积法获得小体积供肝,以探讨大鼠不同体积的原位肝脏模型的建立方法及疗效。一、材料和方法雄性SD大鼠,周龄6～12周,体重2 40g左右。自由进食水,12h昼夜生活环境。采用浓度为0 .6%的苯巴比妥钠,按每公斤体重3 0～5 0mg给予腹腔内注射。全肝脏移植供肝获取按Kamada方法[1] 。5 0 %和3 0 %左右大小的小体积供肝的获取是首先按全肝脏移植时的方法获取全肝,然后,在体外即保存液中依次切取尾状叶,三角叶和左外叶。对于5 0 %体积大小供肝脏移植物,保留肝右叶和肝中叶。对于3 0 %体积大小供肝,要同时切除肝右叶,只保留肝中叶作…     

成人间活体肝移植后小肝综合征的预防：附6例报告

目的：探讨预防成人间活体肝移植术后小肝综合征（SFSS)的方法。 方法：回顾性分析6例成人间活体肝移植(LDLT)的临床资料,包括受体术前血细胞计数、脾脏厚度、门静脉直径、移植物重量与受体体重比（GRWR）、移植物体积与受体标准肝体积比（GV/SLV）及肝静脉重建等,探讨合适体积移植物、良好肝静脉回流、及正常门静脉灌注对SFSS的预防作用。 结果：受体术前均无严重门静脉高压,均没有采用降门静脉压力与血流的措施,6例肝移植物GV/SLV均大于40%,除1例GRWR为0.74%外,余均大于0.8%。6例受体肝静脉重建均良好,重建后肝脏无淤血改变。术后无SFSS发生。 结论：LDLT通过选择合适体积移植物,重建良好的肝静脉回流,控制门静脉压力,防止门静脉过度灌注等有助于预防SFSS的发生。     

大鼠边缘性体积供肝肝移植模型的实验研究

目的通过建立不同体积供肝的大鼠肝移植模型,探索边缘性体积供肝大小的适宜范围,为研究小肝综合征的发病机理及防治措施提供一种易于复制的小动物模型。方法将192只大鼠随机分为全肝移植组、半肝移植组、小体积供肝移植组及超小体积供肝移植组,每组48只,分别建立全肝、半肝、小体积供肝和超小体积供肝的大鼠肝移植模型。移植术后,4组各抽取24只大鼠用于观察存活率;抽取12只大鼠于移植术前,移植术后5、15、30、45及60min测定门静脉压力;另12只大鼠于术后24h测定谷丙转氨酶（ALT）水平。结果全肝移植组的7d累积生存率为100％（24／24）,半肝移植组为87．5％（21／24）,小体积供肝移植组为37．5％（9／24）,超小体积供肝移植组均于术后48h内死亡。全肝移植组术中开放门静脉后,60min内其门静脉压力稳定;半肝移植组大鼠在开放门静脉后,其门脉压力虽有小幅升高,但仍保持相对稳定;而小体积供肝移植组和超小体积供肝移植组开放门静脉后,其门静脉压力均显著升高,15min时均达到高峰,之后该2组的门静脉压力开始回落,至45～60min时逐渐稳定。供肝的体积大小与开放门静脉后5（r=-0．942）、15（r=-0．947）、30（r=-0．900）、45（r=-0．825）和60min（r=-0．705）时的门静脉压力均呈负相关关系（P〈0．001）。肝移植术后24h,全肝移植组和半肝移植组ALT水平均低于小体积供肝移植组及超小体积供肝移植组（P〈0．05）,且小体积供肝移植组ALT水平低于超小体积供肝移植组（P〈0．05）。供肝体积的大小与大鼠移植术后的ALT水平呈负相关关系（r=-0．685,P〈0．001）。结论大鼠部分肝移植模型中,供肝与受体标准肝脏体积比（Gv／sLV）的安全界限为50％,GV／SLV为30％～35％的供肝可视为边缘性体积供肝,小于30％的供肝可视为超小体积供肝。     

劈离式肝脏移植8例

供肝短缺是肝移植手术的制约因素,虽然活体部分供肝、边缘供体增加了供体池,但都存在一定风险,数量也极其有限。劈离式肝脏移植（splitting liver transplantation,SLT）可一定程度上缓解供受者间的矛盾,尤其儿童供肝短缺问题。     

未行门脉血流调整的活体肝左叶移植

成人间活体肝移植（LDLT）中最关键的是要减少供体的手术并发症和死亡率。然而肝右叶移植中供体死亡时有报道。肝左叶移植是降低供体危险的理想选择。然而肝左叶通常太小，可能导致移植术后小肝综合症（SFS）。在西方国家中，肝左叶移植已经放弃，因而缺乏肝左叶移植的临床资料，一般认为SFS形成的重要原因为移植物接受过量门脉血流（PVF）灌注。研究认为当PVF大于260ml／min／100g移植物重量时，移植肝预后较差。尽管已有研究通过脾动脉的结扎、脾切除术或门体分流等方式调控PVF预防移植肝的过度灌注，但仍不清楚移植物的最佳PVF。作者总结了从2004年1月到2007年8月期间未行移植肝门脉血流调整的19例病例资料，分析肝脏血流动力学与移植肝功能和移植结局的关系，阐述不进行门脉血流调整对LDLT中肝左叶移植物的影响。     

辅助性活体部分肝移植治疗一例成人胆道闭锁

活体部分肝移植（LRLT）中常将活体的左外叶或左半肝作为移植肝，但当受体肝脏体积较大，移植肝可能不能提供足以维持生命的肝功能储备。尽管采用活体的右半肝作为移植肝可提供2倍于左半肝的功能体积，但却增加了供者的危险性。因此，近来已开展了辅助性活体部分肝移植术（APOLT）治疗非肝硬变性代谢性肝病的爆发性肝衰。已有报道APOLT有3个优点：1．在移植肝功能严重不全期间，残留原肝可以有继续工作的能力，至整个肝功能逆转。2．对爆发性肝衰病人，移植肝能暂时维持肝功能，使不需免疫抑制的病变原肝有机会恢复功能。3．对有某些…     

活体肝移植后小肝综合征4例

目的:探讨活体肝移植后小肝综合征的病因及其诊治。方法:结合文献,回顾性分析4例小肝综合征的临床特点及治疗经验。结果:4例均有高胆红素血症,2例出现顽固性腹水,最终2例死亡,1例经保守治疗治愈,1例经急诊再次肝移植后治愈。结论:小肝综合征是活体肝移植术后严重并发症,诊治较困难;术前CT评估体积并不能绝对避免小肝综合征的发生;严重者需行再次肝移植。     

活体肝移植术中门静脉血流量检测与调整预防小肝综合征

目的：探讨活体肝移植术（living donor liver transplantation,LDLT）中测定与调整门静脉血流量对小肝综合征（small-for-sizesvndrome,svss）的预防作用。方法：回顾性分析我中心2007年9月至2008年3月行门静脉血流测定的31例LDLT病例资料,包括移植物重量／受体体重（GRWR）、门静脉血流量及术后小肝综合征发生率,探讨检测和调整LDLT中行脾切除及睥动脉结扎病人的门静脉血流量对预防小肝综合征的作用。结果：8例LDLT术中同时行脾切除术,切脾后门静脉血流量较切脾前明显降低（P〈0．01）。5例LDLT术中同时行脾动脉结扎,结扎后门静脉血流量亦较前减低（P=0．017）。行门静脉血流调整组（13例）的GRWR低于未调整组（18例）（P=0．044）;而门静脉血流量则明显高于未调整组（P〈0.001）。调整组无小肝综合征发生,未调整组发生1例小肝综合征。结论：LDLT术中通过脾切除或行脾动脉结扎者降低了移植肝门静脉血流量,有预防术后小肝综合征的作用。监测门静脉血流量为指导门静脉血流调整提供了较客观的依据。     

Review of the surgical approach to prevent small-for-size syndrome in recipients after left lobe adult LDLT

Left lobe liver grafts increase the donor safety in adult-to-adult living-donor liver transplantation (ALDLT). However, the left lobe graft provides about 30–50 % of the required liver volume to adult recipients, which is insufficient to sustain their metabolic demands, which can lead to small-for-size syndrome (SFSS). Transient portal hypertension and microcirculatory hemodynamic derangement, apart from outflow obstruction, during the first week after reperfusion are the critical events associated with small-for-size graft transplantation. The incidence of SFSS in left lobe ALDLT can be decreased by increasing the left lobe graft volume by effective utilization of the caudate lobe with preserved vascular supply, by modulating the portal pressure with splenectomy or a porto-systemic shunt or by hepatic venous outflow reconstruction to prevent the development of venous congestion. In this review, we discuss the pathophysiology of SFSS and the various surgical strategies that can be performed to prevent SFSS in an effort to enhance the donor safety during living-donor liver transplantation.     

Small-for-Size Syndrome After Partial Liver Transplantation: Definition, Mechanisms of Disease and Clinical Implications

Widespread application of cadaveric split or living donor liver transplantation bears considerable potential to increase the pool of available organs and thus alleviate the problem of organ shortage. Although splitting of a cadaveric liver into two grafts for adult recipients can be performed successfully, sufficient function of undersized grafts is a major concern. To minimize the risk for living donors, transplant surgeons aim at procuring the least necessary liver volume, also leading to potentially small grafts. When small partial grafts are unable to meet the functional demands, the recipients can develop a so-called small-for-size syndrome (SFSS). There is currently limited data on the pathogenesis of SFSS, with clinical studies mainly focusing on portal hyperperfusion. Additional aspects include graft-related factors such as functional and regenerative capacity, as well as recipient-related factors, such as overall health status and severity of cirrhosis. However, there is currently no consensus on the definition of SFSS. We propose a novel definition, based on simple clinical criteria, which divides the syndrome into either nonfunction or dysfunction of a small graft after the exclusion of other causes. This definition should ease comparability of future clinical trials, and thus improve understanding of the pathogenesis of SFSS.     

New prediction factors of small‐for‐size syndrome in living donor adult liver transplantation for chronic liver disease

Small‐for‐size syndrome (SFSS), which is characterized by synthetic dysfunction and prolonged cholestasis, is a major cause of worse short‐term prognoses after living donor adult liver transplantation (LDALT). However, the risks of SFSS remain unclear. The aim of this study was to clarify the risks of SFSS, which were analysed in 172 patients who underwent LDALT for chronic liver disease. Graft types included left lobe with caudate lobe graft (n = 110) and right lobe graft (n = 62). Thirty‐four cases (24 with left lobe grafts and 10 with right lobe grafts) were determined as SFSS. SFSS developed even if the actual graft‐to‐recipient standard liver volume ratio was >40%. Logistic regression analysis revealed three independent factors associated with SFSS development in left and right lobe grafts: donor age, actual graft‐to‐recipient native liver volume ratio, and Child’s score. Donor age and actual graft‐to‐recipient native liver volume ratio may become predictive factors for SFSS development in left and right lobe grafts in patients undergoing LDALT.     

Small for size syndrome following living donor and split liver transplantation

The field of liver transplantation is limited by the availability of donor organs. The use of living donor and split cadaveric grafts is one potential method of expanding the donor pool. However, primary graft dysfunction can result from the use of partial livers despite the absence of other causes such as vascular obstruction or sepsis. This increasingly recognised phenomenon is termed "Small-for-size syndrome" (SFSS). Studies in animal models and humans have suggested portal hyperperfusion of the graft combined with poor venous outflow and reduced arterial flow might cause sinusoidal congestion and endothelial dysfunction. Graft related factors such as graft to recipient body weight ratio < 0.8, impaired venous outflow, steatosis > 30% and prolonged warm/cold ischemia time are positively predictive of SFSS. Donor related factors include deranged liver function tests and prolonged intensive care unit stay greater than five days. Child-Pugh grade C recipients are at relatively greater risk of developing SFSS. Surgical approaches to prevent SFSS fall into two categories: those targeting portal hyperperfusion by reducing inflow to the graft, including splenic artery modulation and portacaval shunts; and those aiming to relieve parenchymal congestion. This review aims to examine the controversial diagnosis of SFSS, including current strategies to predict and prevent its occurrence. We will also consider whether such interventions could jeopardize the graft by compromising regeneration.     

Small‐for‐size syndrome in live donor liver transplantation—Pathways of injury and therapeutic strategies

Due to the severe organ shortage and the increasing gap between the supply and demand for donor grafts, live donor liver transplantation (LDLT) has become an accepted and alternative technique for the expansion of the donor pool. However, donor safety and good recipient outcomes must be balanced regarding risk stratification and decision‐making within this patient population. Small‐for‐size syndrome (SFSS) is one of the complications encountered after LDLT, thus increasing the burden of optimizing donor graft selection and effective treatments during its occurrence. A graft‐to‐recipient weight ratio (GRWR) <0.8 predisposes the graft to SFSS. However, other factors may induce this complication even without a graft‐to‐patient size mismatch. Several strategies to prevent this complication include portal vein flow and liver outflow modulation, as well as pharmacological treatment. Also, as an entity with a multifactorial etiology, outcomes vary between right‐lobe, left‐lobe, and posterior‐lobe donation among series encountered in the literature. In this review, we analyze the pathophysiology and classification of this complication, the state‐of‐the‐art on management of SFSS, and the outcomes regarding the best treatment strategy on this patient population.     

活体肝移植小肝综合征的研究进展

目的 探讨在活体肝移植中小肝综合征发生的原因、预防及治疗方法.方法 复习国内、外近几年活体肝移植术后有关小肝综合征的相关报道.结果 供体年龄、脂肪肝程度、受体术前疾病状态(MELD评分)、术后高门静脉灌注、流出道不畅及移植物大小和质量对活体肝移植术后小肝综合征的发生起着重要作用,术前选择最佳的供体,术中的脾脏切除或脾动脉结扎或对门静脉限流,保证流出道的绝对通畅,术后及早发现并积极治疗能显著减少小肝综合征的发生.结论 小肝综合征的危险因素是可以预测的,积极的应对措施可以用于小肝综合征的预防与治疗.     

小肝综合征(SFSS)的研究进展

小肝综合征(small-for-size syndrome,SFSS)是成人间活体肝脏移植(living donor liver transplantation,LDLT)最严重的并发症,也是成人间LDLT预后差的重要原因,其确切概念和发病机制尚未统一,存在广泛的争议.本文对其主要发病机制的研究进展作了概括,归纳了相关预防和治疗方案,包括:术前供者和移植物的选择、降低门静脉高灌注、双肝移植技术的应用、分子药物的应用及其他创新技术的使用等五个方面.同时,对其未来的研究方向提出了相关见解.

Abstract：

The small-for-size syndrome (SFSS) is widely recognized as one of the most serious clinical complications. It substantially contributes to a poor prognosis after adult living donor liver transplantation. Currently, there is still no consensus on the exact definition and pathogenesis of SFSS. We reviewed the progress on research of pathogenesis of SFSS and put forward some relevant preventive and treatment measures, including donor selection, graft assessment, reduction of high portal vein perfusion, dual grafts technology, advanced molecular medicine and other innovative approaches. Also, we offered some relevant insights into the future research directions of SFSS.