大鼠肝移植重建肝动脉对胆管超微结构和并发症的影响

目的 观察大鼠原位肝移植重建肝动脉对肝内胆管上皮细胞缺血再灌注损伤后超微结构及术后胆道并发症的影响.方法 228只SD大鼠分为假手术组(8只)、肝移植重建肝动脉组(55对)和未重建肝动脉组(55对).重建肝动脉组和未重建肝动脉组分别于肝脏复流后0.5、3、6、12、24、36、48 h取材,用透射电镜观察肝内胆管上皮细胞的超微结构,通过计算机图像分析系统对线粒体形态计量分析;观察术后胆道并发症.结果 两组肝内胆管上皮细胞损伤均有加重,表现为线粒体肿胀、嵴模糊或消失、微绒毛减少等超微结构改变,至24 h达高峰,以后逐渐恢复.术后两组线粒体平均面积和周径随时间的延长逐渐增大,线粒体数密度随时问延长而减少.在24 h,两组缺血再灌注损伤最显著,之后均开始缓解.在24、36、48 h,两组线粒体平均面积、平均周径比较,差异均有统计学意义(t=-3.566,-7.780,-4.730,-4.610,-2.599,-5.370,P＜0.05);在36、48 h,两组线粒体平均数密度比较,差异有统计学意义(t=-4.619,4.000,P＜0.05).重建肝动脉组的胆道并发症发生率低于未重建肝动脉组(x2=4.286,P＜0.05).结论 大鼠肝移植重建肝动脉对肝内胆管上皮细胞缺血再灌注损伤后的超微结构具有保护作用,有利于术后恢复和减少胆道并发症的发生.     

缺血预处理对胆管上皮细胞凋亡及bcl-2/Fas蛋白表达的影响

目的 观察缺血预处理对缺血再灌注损伤引起的胆管上皮细胞凋亡(AI)以及对调控基因(bcl-2,Fas)蛋白表达的影响. 方法 SD大鼠36只分为假手术(SO)组、缺血再灌注(IR)组、缺血预处理(IP)组.热缺血时间为30min.缺血预处理为缺血前采用5 min缺血及5 min×2次再灌注.分别于再灌注12 h后处死动物取肝脏标本.检测肝内胆管上皮细胞凋亡及bcl-2/Fas蛋白表达水平. 结果 凋亡细胞主要见于肝内大胆管,SO组凋亡的胆管上皮细胞罕见,IR和IP组与SO组比较,胆管上皮细胞AI有显著性增加(P<0.01,P<0.05).IP组与IR组比较,胆管上皮细胞AI有显著性降低(P<0.05).肝内大胆管bcl-2蛋白阳性表达:IP组bcl-2蛋白阳性表达较SO组和IR组差异均具有显著性意义(P<0.01,P<0.05).Fas蛋白阳性表达:IR组与SO组比较,Fas蛋白阳性表达差异有显著性意义(P<0.05).IP组与IR组间相比差异无显著性意义(P>0.05). 结论 IR诱导Fas蛋白的表达促进肝内胆管上皮细胞发生凋亡.IP通过上调调控基因bcl-2蛋白的表达抑制胆管上皮细胞的凋亡,与Fas蛋白表达关系不明显.     

亲水性胆盐对减轻大鼠移植肝肝内胆管冷保存再灌注损伤的作用

目的 探讨亲水性胆盐对减轻大鼠移植肝肝内胆管冷保存再灌注损伤的作用.方法 应用大鼠原位肝移植胆道外引流模型,将192只SD大鼠随机分为4组,每组供、受者各24只.各组供者在供肝切取前30 min经阴茎背静脉注射不同的试剂,对照组注射1 ml生理盐水;疏水性胆盐(TDC)组注射牛磺脱氧胆酸钠40/μmol/kg;高、低浓度亲水性胆盐(TUDC)组分别注射牛磺熊去氧胆酸钠80和40μmol/kg.供肝取出后置于4℃的平衡液中保存2 h再植入受者.移植肝再灌注后1、3、7和(或)14 d时,采用全自动生化分析仪分别检测受者血清中碱性磷酸酶、γ-谷氨酰转移酶、胆红素总量、直接胆红素和胆汁中γ-谷氨酰转移酶和葡萄糖的含量.移植肝再灌注后1 d时,在光镜下观察肝内胆管上皮细胞的病理学改变,在荧光显微镜下观察肝内胆管上皮细胞的凋亡情况.结果 高、低浓度TUDC组各项观察指标均低于对照组和TDC组(P＜0.05),且肝内胆管炎症细胞的浸润、上皮细胞的损伤以及细胞的凋亡等程度均轻于对照组和TDC组(P＜0.05);与低浓度TUDC组比较,高浓度亲水性胆盐组短期内可见各项观察指标均有所降低,但远期各指标的比较,差异无统计学意义(P＞0.05).TDC组术后各项观察指标均高于对照组(P＜0.05).结论 在供肝获取前,供者静脉注射亲水性胆盐能减轻大鼠移植肝肝内胆管的冷保存再灌注损伤.     

胆管上皮细胞分泌的VEGF-A在热缺血再灌注损伤后胆道及其微循环再生与修复中的作用

目的 探讨热缺血再灌注损伤后血管内皮生长因子-A(vascular endothelial growth factor-A,VEGF-A)在胆道及其微循环再生与修复中的作用,为积极预防和治疗胆道热缺血再灌注损伤导致的胆道并发症提供理论依据.方法 供受体均为雄性SD大鼠.供肝分别经历0 min(对照组)和10 min(实验组)热缺血后,进行重建肝动脉血供的大鼠肝移植模型.分别于供肝冷保存后(即0 h)以及术后6 h、24 h、3 d、7 d、14 d、30 d处死大鼠,收集标本.测定血清ALT、GGT、TBIL.免疫组化法检测VEGF-A表达情况.分别标记胆管上皮细胞、血管内皮细胞、增殖细胞,统计汇管区胆管数、血管数以及胆管上皮细胞增殖指数.原位杂交法检测VEGF-A mRNA表达情况.结果 实验组GGT和TBIL较对照组升高持续时间更长,术后30 d和14 d才降至正常.实验组汇管区胆管数及血管数均在术后14 d达到最高值,且明显多于对照组.肝细胞和血管内皮细胞VEGF-A、VEGF-AmRNA表达在术后24 h达到峰值后迅速下降,而胆管上皮细胞VEGF-A、VEGF-A mRNA表达持续升高,直到术后7 d才达到峰值.并且实验组表达水平均强于相应时间点对照组的表达.结论 热缺血再灌注损伤后.胆管上皮细胞合成和分泌VEGF.A增加,并且可能在促进胆管及胆管周围血管丛的再生中发挥重要作用.     

肝门阻断时肝动脉与门静脉不同开放时序对肝脏缺血再灌注的影响

目的 研究大鼠肝脏热缺血后经门静脉和肝动脉不同时序灌注对其损伤的影响,探索是否可由此减轻大鼠肝脏缺血再灌注损伤及其可能的机理.方法 选用健康雄性SD大鼠96只,按随机数字表法等分成6组,1组为假手术组,其余5组为实验组.假手术组(16只)只作开腹和肝门部解剖; 实验组(共5组,每组16只)根据再灌注时门静脉和肝动脉不同开放时序分组: 先开放门静脉1 min后再开放肝动脉组、先开放门静脉2 min后再开放肝动脉组、先开放肝动脉1 min后再开放门静脉组、先开放肝动脉2 min后再开放门静脉组及同时开放门静脉和肝动脉组.各组分别于术后2 h和4 h检测血清中ALT和AST值,肝组织中丙二醛(MDA)、超氧化物歧化酶(SOD)及谷胱甘肽(GSH)含量变化; 采用病理组织切片HE染色观察肝组织损伤情况; TUNEL法检测各组肝组织细胞凋亡情况.结果 假手术组大鼠肝脏基本正常,各指标均好于各实验组,差异均有统计学意义(P＜0.01).在各实验组中先开放门静脉1 min后再开放肝动脉组大鼠肝脏缺血再灌注损伤最轻,其ALT、AST、MDA和凋亡指数值均明显低于其他各实验组,差异有统计学意义(P＜0.05或P＜0.01),并且其SOD和GSH值均高于其他各实验组,差异亦有统计学意义(P＜0.05或P＜0.01).肝组织HE染色也显示,先开放门静脉1 min后再开放肝动脉组大鼠肝组织损伤较其他各实验组轻.结论 肝脏热缺血后,通过短暂开放门静脉再开放肝动脉的措施可以减轻大鼠肝脏缺血再灌注损伤,可能与降低活性氧的产生及保护肝脏抗氧化系统有关.     

普通超声及超声造影检测兔胆道缺血模型胆道异常的可行性研究

目的探讨普通超声及超声造影应用于检测兔胆道缺血模型胆道异常的可行性。方法将20只健康新西兰兔随机分为两组,对照组及肝动脉和胆总管联合阻断2h(HBO2h)组(各10只)。HBO2h组用无损伤动脉夹阻断肝动脉及胆总管下段2h后去除动脉夹制作胆道缺血模型,对照组不进行任何手术处理。术后5d两组实验兔先后采用普通超声、超声造影观察胆总管-左叶胆管情况,然后处死动物取胆总管-左叶胆管标本行苏木素-伊红(HE)染色,对胆管组织缺血损伤程度进行评分,CD34免疫组织化学染色后行微血管密度(microvascular density,MVD)定量分析。结果普通超声表现:对照组门静脉管径/胆管管径比值为3.47±0.23,所有胆管(100%)均表现为管壁连续性好、无增厚,管腔清晰;HBO2h组胆管明显扩张,门静脉管径/胆管管径比值为1.25±0.42,与正常组比较差异有统计学意义(P<0.01);所有胆管均表现为管壁毛糙、增厚。超声造影表现:对照组所有胆管壁(100%)较肝实质提早增强,动脉期胆管壁呈细线状高增强,门静脉期及延迟期呈等增强;HBO2h组中60%(6/10)表现为动脉期胆管壁呈增强水平明显降低,门静脉期及延迟期呈低增强;40%(4/10)表现为增强扫描全过程均呈无增强;与对照组相比,HBO2h组各时相胆管壁增强表现差异均有统计学意义(均为P<0.05)。病理学表现:对照组胆管黏膜上皮细胞和黏膜下腺体上皮细胞呈柱状,排列紧密、完整,无上皮细胞变性、坏死、脱落等,胆管损伤评分为0分,MVD为(6.1±2.5)个。HBO2h组胆管壁增厚,胆管黏膜上皮细胞及黏膜下腺体上皮变性、坏死、脱落,管壁炎症细胞浸润,胆管损伤评分为(2.1±0.6)分,MVD为(2.2±1.6)个,与对照组比较差异有统计学意义(均为P<0.01)。结论普通超声及超声造影能较早发现胆道缺血兔模型的胆道异常,为缺血型胆道病变动物实验研究提供了一种简便、无创、动态监测病程发展的有效手段。     

不同胆道灌洗方法对大鼠肝内胆管冷保存再灌注损伤的影响

目的观察不同胆道灌洗方法对大鼠移植肝肝内胆管冷保存再灌注损伤的影响。方法应用大鼠原位肝移植模型，将88只SD大鼠随机分为假手术组、胆道非灌洗组、UW液胆道灌洗组、生理盐水（NS）胆道灌洗＋UW液肝内胆道灌注保存组、HTK液胆道灌洗＋UW液肝内胆道灌注保存组、HTK液胆道灌洗＋HTK液肝内胆道灌注保存组。移植肝置于4℃林格液中保存2h后行原位肝移植。移植肝再灌注后24h，检测血清总胆红素（TB）、直接胆红素（DB）、碱性磷酸酶（AKP）、γ-谷酰转肽酶（GGT）及胆汁中GGT、葡萄糖（Glu）含量。在光镜及电镜下观察肝内胆管上皮细胞的形态学变化。结果与非灌洗组比较，胆道灌洗组术后各项指标明显改善（P〈0．01）；HTK液及NS灌洗组较UW液灌洗组术后指标改善明显（P〈0．05）。病理检测发现非灌洗组胆道损伤明显，各灌洗组胆道损伤程度明显改善，HTK液灌洗＋UW或HTK液灌注组对胆管上皮细胞的损伤较轻。结论移植肝冷保存前进行胆道灌洗可以明显减轻胆管上皮细胞的损伤，4℃HTK液灌洗＋4℃UW或HTK液灌注保存效果比较理想。     

胆总管结扎预适应减轻小鼠肾脏缺血再灌注损伤

目的 探讨胆总管结扎预适应减轻小鼠肾脏缺血再灌注损伤的可能机制.方法 C57BL/6小鼠分为3组进行实验.胆总管结扎预适应组(CBDL组)结扎胆总管(d0),2d后(d2)再通,再过2d后(d4)行左肾缺血再灌注手术;假手术组仅结扎胆囊管(d0),d4再行左肾缺血再灌注手术;对照组不进行任何处理.监测血胆红素总量(TBil)的变化情况.肾脏缺脏再灌注后24 h(dS)检测各组小鼠血清肌酐(Cr).蛋白质印迹法检测CBDL组和假手术组肾脏热休克蛋白27 (HSP-27)和内皮型一氧化氮合酶(eNOS)的表达情况.结果 CBDL组胆总管结扎2d后,TBil达到最高,再通2d后,TBil基本降至正常水平.CBDL组Cr低于假手术组(P＜0.05).CBDL组HSP-27和eNOS的表达量高于假手术组(P＜0.05).结论 胆道结扎预适应能明显减轻小鼠肾脏缺血再灌注损伤,其机制可能与引起肾脏局部HSP-27和eNOS高表达有关.     

胆管周围血管丛在移植肝胆道热缺血再灌注损伤与修复中的作用

目的 探讨热缺血再灌注损伤后胆管周围血管丛在胆道损伤与修复中的作用,及胆道易受热缺血再灌注损伤的可能机制.方法 雄性SD大鼠,随机分为3组:假手术组(S组);无热缺血组(W0组);10 min热缺血组(W 0组).分别在冷保存后(即0 h)及移植肝再灌注后6,24 h,3,7,14,30 d获取标本.每个时间点6只.检测各组血中ALT,GGT,TBIL.并取肝组织行连续切片,分别利用CK19和第八因子相关抗原标记胆管上皮细胞和血管,计数每个汇管区胆管、血管、伴有血管的胆管、不伴有血管的胆管以及孤立的血管数.结果 W10组GGT,TBIL比W0组GGT,TBIL高于S组的时间更长,且ALT恢复至S组水平较GGT,TBIL更早、更快.W10组汇管区炎症细胞浸润程度、胆管结构破坏程度、汇管区纤维化,比WO组及S组更严重.电镜下可见,W10组胆管周围血管丛内微血栓形成.肝移植术后6,24 h,W10组移植肝汇管区血管数量较W0组及S组明显减少.虽然术后24 h胆管即开始明显增生,但直到术后14～30 d,W10组血管数及伴有血管的胆管数才较W0组及S组增多.结论 移植肝热缺血再灌注损伤可致胆管周围血管丛微血栓形成,引起血管内皮细胞损伤加重,导致胆管微循环障碍,以及胆管周围血管丛再生明显滞后于胆管再生,这些可能是胆管易受热缺血再灌注损伤的重要原因.     

内质网应激分子伴侣GRP78在大鼠缺血再灌注损伤肝脏中的表达

目的:观察内质网应激相关分子葡萄糖调节蛋白78(GRP78)在大鼠缺血再灌注损伤肝脏组织中的表达水平.方法:将24只健康雄性SD大鼠随机均分为假手术组,单纯肝缺血组(肝缺血30 min+再灌注0h),再灌注6h组(肝缺血30 min+再灌注6h)和再灌注12h组(肝缺血30 min+再灌注12h).分别检测各组血清丙氨酸转氨酶(ALT)和门冬氨酸转氨酶(AST)水平;肝组织病理学、凋亡情况及GRP78 mRNA表达水平.结果:与对照组比较,各实验组大鼠肝缺血后出现明显的肝组织损伤,且随着再灌注时间的延长损伤加重,表现为血清ALT和AST水平升高,明显的肝组织病理学改变,肝细胞凋亡率增加,各组间计量指标的差异均有统计学意义(均P＜0.05).大鼠肝组织GRP78 mRNA变化趋势与上述指标一致,缺血后表达明显上调,且随着再灌注时间延长而逐渐升高,各组间差异均有统计学意义(均P＜0.05).结论:缺血再灌注损伤肝脏组织中GRP78表达上调,但其具体作用还有待于探明.     

Intrahepatic biliary strictures after liver transplantation

Biliary complication has been one of the most common complications after liver transplantation. Nonanastomotic strictures and dilatations involving the intrahepatic biliary tree have been recognized as biliary complications. These lesions were reported to be associated with hepatic artery thrombosis; prolonged preservation time; ABO-incompatible organs; and immunological injury, including injuries to vascular endothelial cells (chronic rejection) and the bile duct (primary sclerosing cholangitis). However, the etiology of these lesions appeared to be mostly related to ischemic injury. Anatomical research on the arterial supply of the bile duct has provided further insights into bile duct blood supply and its surgical implications. The biliary tract is supplied with arterial blood by a vasculature called the peribiliary vascular plexus. Any injury to the peribiliary vascular plexus may contribute to ischemic death of the biliary system mucosa. At many points, the process of liver transplantation exposes the endothelial cells and peribiliary vascular plexus to ischemic injury. The majority of intrahepatic biliary strictures (IHBS) are diffuse or bilateral. A percutaneous or an endoscopic approach has been used as the initial treatment. However, a low threshold for surgical intervention (retransplantation) should be adopted, because these patients demonstrate high mortality. The aim of this article is to review the anatomy, etiology, clinical picture, diagnosis, management, and prognosis of IHBS after liver transplantation.     

中华眼镜蛇毒抑制肾缺血再灌注损伤的实验研究

目的 探讨中华眼镜蛇毒(CCV)对大鼠肾缺血再灌注(I/R)损伤的肾保护作用及其机制。方法 雄性SD大鼠32只,随机分为4组。Ⅰ、Ⅱ组建立肾I/R模型, 分别于再灌注前0.5 h、12 h腹腔注射0.1% CCV(0.4 mg/kg); Ⅲ组制备肾I/R模型作病理对照; Ⅳ组为假手术组。应用苦味酸法和二乙酰一肟法分别测定大鼠缺血前、再灌注24 h的Scr和BUN值。用免疫比浊法测定再灌注0、0.5、2、24 h的血清补体C3水平。HE染色光镜下观察肾组织损伤形态学改变,并利用原位凋亡检测法(TUNEL)检测细胞凋亡情况。结果 再灌注后24 h的Scr和BUN值在Ⅱ组明显降低,与Ⅰ、Ⅲ组相比差异有统计学意义(P < 0.05)。补体C3水平在Ⅱ组于再灌注0 h显著降低,与其他组0 h时比较,差异均有统计学意义(P < 0.05);Ⅰ、Ⅲ组C3于再灌注2 h明显下降,与再灌注0 h比较,差异有统计学意义(P < 0.05)。HE染色可见Ⅰ、Ⅲ组损伤较重,以近端小管变性,坏死为主;Ⅱ组病变明显减轻。在Ⅲ和Ⅰ组均可见大量TUNEL阳性细胞,而在Ⅱ组其数量与上两组相比显著减少(P < 0.05)。结论 肾I/R可明显引起肾组织损伤和功能损害。再灌注前12 h用CCV预处理大鼠,能够明显降低补体C3, 从而有效抑制补体介导的肾I/R损伤。     

辛伐他汀对肺缺血再灌注损伤中肺泡Ⅱ型细胞的保护作用

目的 观察辛伐他汀对大鼠肺缺血再灌注损伤(LIRI)长期存活模型中肺泡Ⅱ型细胞(ATⅡ)的保护作用.方法 建立大鼠肺缺血再灌注损伤长期存活模型,将实验动物分成3组:假手术组(Ⅰ组,仅予开胸,n=36)、缺血再灌注组(Ⅱ组,予左侧肺门阻断1 h后开放,n=36)、辛伐他汀组(Ⅲ组,术前3 d开始予辛伐他汀每天5 mg/kg灌胃持续应用至处死,余处理同Ⅱ组,n=36).分别于开胸后及缺血再灌注后0 h、4 h、1 d、3 d、7 d收集血及左肺组织标本,检测如下指标:血氧分压(PaO2)、组织髓过氧化物酶(MPO)水平、肺组织肺泡表面活性物质C(SP-C)表达及SP-C/增殖细胞核抗原(PCNA)免疫荧光双染检测ATⅡ的增殖.结果 成功建立大鼠肺缺血再灌注损伤长期存活模型.与Ⅱ组比较,Ⅲ组MPO值、PaO2值以及SP-C的mRNA相对值在缺血再灌注4 h和1 d差异均有统计学意义(P＜0.01),余时间点差异均无统计学意义(P＞0.05);SP-C/PCNA免疫荧光双染显示,Ⅲ组在缺血再灌注后1 d ATⅡ增殖水平较Ⅱ组明显增高.结论 ATⅡ细胞是辛伐他汀保护肺缺血再灌注损伤作用的新靶点,促进其增殖是辛伐他汀发挥保护作用的重要机制之一.

Abstract：

Objective To evaluate the protective effects on alveolar type Ⅱ cells induced by simvastatin in a rat lung ischemia-reperfusion injury (LIRI) long-term survival model. Methods 108 healthy SD rats were randomly divided into 3 groups: group Ⅰ, the sham group (n =36, no hilar blocking); group Ⅱ, LIRI group ( n = 36, left hilar blocking); group Ⅲ, simvastatin group ( n = 36, animals were orally lung tissue and blood samples were collected at basehne before hilar occlusion and 1 h after ischemia, 4 h,1 day, 3 days and 7 days after reperfusion respectively. The indices were determined as follows: the myeloperoxidase (MPO) activity of lung tissue, the arterial partial pressure of oxygen ( PaO2 ), pulmonary surfactant-C (SP-C) expression and proliferation of AT Ⅱ cells determined by SP-C/proliferating cell nuclear antigen (PCNA) immunofluorensence double staining. Results The rat LIRI long-term survival model was successfully established. As compared with group Ⅱ , the MPO activity, PaO2 and the SP-C mRNA level were significantly reduced in group Ⅲ at the time-points of 4 h and 1 day after reperfusion (P ＜0. 01 respectively). The number of SP-C/PCNA double positive AT Ⅱ cells displayed that as compared with Group Ⅱ , the proliferation of AT Ⅱ cells in group Ⅲ was significantly increased at day 1 after repeffusion.Conclusion AT Ⅱ cells might be a novel target of simvastatin-induced-attenuation of LIRI, in which enhancing the proliferation ability of AT Ⅱ is involved as one of the important mechanisms.     

肝移植术后并发高位胆管狭窄的原因及诊治八例

目的 探讨原位肝移植术后并发高位胆管狭窄的原因及诊治.方法 对8例肝移植后并发高位胆管狭窄患者的资料进行回顾性分析,8例均行背驮式肝移植,胆管采取端端吻合,其中2例置婴儿胃管.结果 高位胆管狭窄发生于术后3～18个月,5例以阻塞性黄疸为主要临床表现,3例以慢性胆管炎为主要临床表现.经保守治疗无效后,均行手术治疗,切除肝门部胆管狭窄段,再行胆肠Roux-en-Y吻合术.手术治疗后随访1～5年,除1例患者因肝癌复发死亡外,其余患者均生存良好.结论 胆道缺血、胆汁腐蚀以及保存性损伤是并发高位胆管狭窄的主要因素;B型超声波和磁共振胰胆管成像是有效诊断手段;胆肠Roux-en-Y吻合是处理高位胆管狭窄的有效方法.     

The blood supply of the biliary ductal system and its relevance to vasculobiliary injuries following cholecystectomy.

BACKGROUND: Cholecystectomy remains the only satisfactory treatment for symptomatic gall bladder stones. Unfortunately, in some cases the operation is complicated by vasculobiliary injury. The present study was undertaken to investigate the blood supply of the normal biliary system, to simulate vasculobiliary injuries described after cholecystectomy, and to determine the possible effects of the vascular injury on biliary reconstruction. METHODS: The blood supply of the biliary system in nine normal livers was investigated by injection of the coeliac axis and superior mesenteric arteries with coloured gelatin. The specimens were dissected under magnification and drawings prepared. Injection dissection studies were also carried out in eight specimens in which various vasculobiliary injuries encountered after cholecystectomy were simulated. RESULTS: The bile ducts possess an arterial plexus on their surface which is supplied from below by ascending marginal vessels derived from the postero-superior pancreaticoduodenal artery. These marginal vessels end above in the right hepatic artery or its branches. The right and left hepatic ductal systems are supplied by the right and left hepatic arteries and their sectoral or segmental branches. The right and left hepatic arteries communicate freely via the hilar plate arterial plexus. This collateral system allows the blood supply to the right hepatic duct to be maintained after ligation of the right hepatic artery and interruption of the common hepatic duct or excision of the confluence. CONCLUSION: A knowledge of the blood supply of the normal biliary system and the collateral hilar plate arterial plexus forms the anatomical foundation for successful reconstructive surgery, not only in vasculobiliary injuries following cholecystectomy, but also for a wide range of hepatobiliary procedures.     

Ⅲ型肝门部胆管癌的外科治疗（附35例分析）

目的总结Ⅲ型肝门部胆管癌的手术经验。方法回顾性分析我院1999年1月至2006年12月，行手术切除的35例Ⅲ型肝门部胆管癌的临床资料。Ⅲa型16例，行肝门部胆管切除8例，行联合右半肝＋右侧尾状叶切除7例，行联合右半肝＋尾状叶切除、门静脉分叉部切除主干左支吻合1例。Ⅲb型19例，行肝门部胆管切除8例，行联合左半肝＋左侧尾状叶切除9例，行联合左半肝＋尾状叶切除、门静脉分叉部切除主干右支吻合1例．行联合左半肝＋尾状叶切除、门静脉分叉部切除主干右支吻合、肝固有动脉分叉部切除主干右支吻合1例。结果本组32例获得随访，随访时间18～113个月。肝门部胆管切除病例术后病理根治性切除率为37．5％，联合肝叶切除病例术后病理根治性切除率73．7％，3例联合肝叶切除＋血管切除病例均获术后病理根治性切除。肝门部胆管切除术后并发症发生率为31．3％，联合肝叶切除组术后并发症发生率为31．6％。3例联合肝叶切除＋血管切除病例术后均无胆肠吻合口漏、肝断面坏死、胆漏等严重并发症。结论联合肝叶切除，必要时行受累分叉部血管切除重建，有益于提高Ⅲ型肝门部胆管癌的根治性切除率，且不增加术后并发症的发生率。     

THE BLOOD SUPPLY OF THE BILIARY DUCTAL SYSTEM AND ITS RELEVANCE TO VASCULOBILIARY INJURIES FOLLOWING CHOLECYSTECTOMY

Background : Cholecystectomy remains the only satisfactory treatment for symptomatic gall bladder stones. Unfortunately, in some cases the operation is complicated by vasculobiliary injury. The present study was undertaken to investigate the blood supply of the normal biliary system, to simulate vasculobiliary injuries described after cholecystectomy, and to determine the possible effects of the vascular injury on biliary reconstruction. Methods : The blood supply of the biliary system in nine normal livers was investigated by injection of the coeliac axis and superior mesenteric arteries with coloured gelatin. The specimens were dissected under magnification and drawings prepared. Injection dissection studies were also carried out in eight specimens in which various vasculobiliary injuries encountered after cholecystectomy were simulated. Results : The bile ducts possess an arterial plexus on their surface which is supplied from below by ascending marginal vessels derived from the postero-superior pancreaticoduodenal artery. These marginal vessels end above in the right hepatic artery or its branches. The right and left hepatic ductal systems are supplied by the right and left hepatic arteries and their sectoral or segmental branches. The right and left hepatic arteries communicate freely via the hilar plate arterial plexus. This collateral system allows the blood supply to the right hepatic duct to be maintained after ligation of the right hepatic artery and interruption of the common hepatic duct or excision of the confluence. Conclusion : A knowledge of the blood supply of the normal biliary system and the collateral hilar plate arterial plexus forms the anatomical foundation for successful reconstructive surgery, not only in vasculobiliary injuries following cholecystectomy, but also for a wide range of hepatobiliary procedures.     

胆道支架联合PTCD对恶性梗阻性黄疸患者肝功能与生活质量的影响研究

目的研究胆道支架联合PTCD对恶性梗阻性黄疸患者肝功能与生活质量的影响。方法随机选取2006年4月至2016年4月期间在我院肝胆外科就诊的恶性梗阻性黄疸的患者216例为研究对象,均采用胆道支架联合PTCD治疗,分析患者胆管狭窄部位及原因,术前3d、术后3d、7d和14d肝功能指标:白蛋白、丙氨酸转氨酶、总胆红素、直接胆红素和间接胆红素,术后并发症及随访结果,对术前感染、肝功能评分和术后针对肿瘤治疗进行多因素COX模型回归分析,采用SPSS20.0统计学软件进分析。结果 (1)肝管癌患者有87例,其中,胆总管60例,肝门部胆管12例,左右肝管15例;胰腺癌患者有35例,狭窄原因为胆总管;肝癌患者有25例,其中,胆总管11例,肝门部胆管6例,多部位8例;壶腹周围癌患者有30例,狭窄原因为胆总管;胃癌肝转移患者有39例,其中,肝门部胆管23例,多部位16例。(2)术后3d、7d和14d的白蛋白、碱性磷酸酶、丙氨酸转氨酶、总胆红素、直接胆红素和间接胆红素含量水平均低于术前,术前后的比较有统计学差异(P0.05);随着术后时间的延长,白蛋白、碱性磷酸酶、丙氨酸转氨酶、总胆红素、直接胆红素和间接胆红素含量水平逐渐降低,趋于正常值范围。(3)胆道感染的患者有17例,发生率为7.87%;急性胰腺炎的患者有21例,发生率为9.72%;支架脱落移位的患者有6例,发生率为2.78%;本组216例患者获访,随访时间为8d-120个月,平均每3个月随访一次,随访期间,有171例患者死亡,均死于肿瘤进展及多脏器功能衰竭,45例患者至随访截止时无黄疸加重症状。(4)术前感染、肝功能评分和术后针对肿瘤治疗是恶性梗阻性黄疸发生的独立因素(P0.05)。结论胆道支架联合PTCD是恶性梗阻性黄疸治疗的有效方法,能提高患者肝功能和改善生活质量,延长生存期。     

腹腔镜胆囊切除术中Mirizzi综合征的诊断、处理及疗效分析

目的探讨腹腔镜胆囊切除术(laparoscopic cholecystectomy,LC)中Mirizzi综合征的诊断、处理方法及疗效。方法我院2003年10月～2010年9月行LC时发现Mirizzi综合征22例,对术中诊断、手术方式及治疗效果进行总结。结果按Csendes分型,Ⅰ型13例,Ⅱ型6例,Ⅲ型2例,Ⅳ型1例。14例完成LC,均为Ⅰ～Ⅱ型病例。中转开腹手术8例。术前行ERCP检查7例,均未发生胆管损伤;术中胆管损伤6例,2例行胆管端端吻合术,4例行胆管瘘口修补术。1例Ⅳ型分离困难中转开腹,胆总管中下段缺失行胆肠吻合术,T管支撑引流术,术后半年拔除T管后,患者有反复发热症状,经保守治疗1年后症状不能完全缓解,再次手术行肝脏右后叶切除术及肝门部胆管成形+胆肠吻合内引流术。结论 Mirizzi综合征诊断困难,腹腔镜手术时易发生胆管损伤等并发症,术前ERCP有利于明确诊断,减少并发症;部分Ⅰ～Ⅱ型患者可以腹腔镜下完成手术;根据术中不同情况选择不同的手术方式,可收到良好的治疗效果。     

Solitary Extra-Hepatic Hilar Peribiliary Cyst Presenting with Obstructive Jaundice: A Case Report

Peribiliary cyst is a poorly recognized and under-reported clinico-pathologic entity around the biliary tree. Peribiliary cysts are cystic dilatations of obstructed peribiliary glands, which are normal elements of the biliary tract. They are generally asymptomatic and rarely cause biliary obstruction. They are usually discovered incidentally at autopsy or in explants following liver transplantation.

A 59-year-old male patient presenting with obstructive jaundice due to a large extra-hepatic hilar peribiliary cyst is reported here. We briefly discuss its differential diagnoses such as bile duct cyst, liver cyst or lymph cyst, and its management.

Radiological imaging demonstrated a solitary large (5 cm) well-defined, smooth, thin walled cystic lesion at the porta hepatis paralleling but not communicating with the bile duct. A wide cyst de-roofing was performed and histological examination of the cystic wall revealed an inflammatory cyst.

The patient made an uneventful recovery and remained asymptomatic with normal liver function tests 36 months post-operatively.