猪急性缺血性肝衰模型的建立和辅助性异位部分肝移植的作用

目的: 探讨急性缺血性肝衰模型的制备、辅助性异位部分肝移植的作用. 方法: 用家猪配对开展辅助性异位部分肝移植.分三组,A组:受体肝脏和肝动脉保持原状,其门静脉缩窄;供肝植入受体右肝下,仅建立门静脉血供,不建立动脉血供.B组:受体肝动脉结扎,其他手术内容与A组相同.C组:受体肝动脉结扎,供肝动脉和门静脉血供均建立,其他手术内容与A组相同.监测各组受体存活情况,肝功能和肝脏血流情况,病理及供肝胆汁分泌情况. 结果: A组、C组受体3 d以上成活率显著高于B组.A组、C组手术前后胆红素无显著改变,B组术后胆红素显著高于术前,术后第二天B组胆红素显著高于A组、C组.C组供肝胆汁分泌和血供良好,肝细胞存活并有活跃的代偿性增生;A组、B组供肝无或仅有少量胆汁分泌,肝细胞大片坏死. 结论: 受体肝动脉结扎、门静脉缩窄足以造成急性肝衰模型;保留受体肝脏动脉血供、减少门静脉血供对受体肝脏功能无严重影响;辅助性异位部分肝移植能取得良好的效果,足以纠正急性肝衰.     

一种大鼠门静脉高压脾功能亢进模型的建立

目的通过门静脉缩窄联合脾静脉结扎的方法,建立大鼠门静脉高压脾功能亢进模型。方法 60只健康雄性SD大鼠按随机数字表法分为假手术组(n=20)、门静脉缩窄组(缩窄组,n=20)和门静脉缩窄联合脾静脉结扎组(联合组,n=20),其中假手术组仅予以开、关腹术,缩窄组予以单纯门静脉主干缩窄术,联合组予以门静脉缩窄联合脾静脉结扎术。造模开始前和造模后7周每周采各组动物外周血行红细胞、白细胞及血小板计数动态观察;于造模开始前和造模后第7周测量各组动物门静脉压力及脾横、长径,于造模后第7周处死动物后计算各组脾指数并观察脾脏组织的病理学变化。结果联合组大鼠外周血血小板及红细胞计数于第3周起明显低于假手术组及缩窄组(P<0.05);而3组白细胞计数各时相间差异均无统计学意义(P>0.05)。第7周时缩窄组及联合组门静脉压力均较术前明显升高(P<0.05),并且明显高于假手术组(P<0.05)。第7周时联合组的脾横径及脾长径较术前明显增大(P<0.05),并且明显大于假手术组及缩窄组(P<0.05),其脾指数亦高于假手术组及缩窄组(P<0.05)。第7周时联合组脾脏有典型的脾功能亢进的病理改变,而另2组未见明显病理改变。结论通过门静脉缩窄联合脾静脉结扎的方法,成功建立了大鼠继发性门静脉高压脾功能亢进模型,该方法手术操作简便、效果稳定,具有良好的科研应用价值。     

肝前性门静脉高压大鼠门静脉血流对肝脏影响的实验观察

目的 研究肝前性门静脉高压大鼠门静脉血流改变对肝脏功能的影响.方法 雄性Wistar大鼠66只,完全随机化分为5组:门静脉部分缝扎组(A组,n=20);部分门静脉、肝动脉顺序缝扎组(B组,n=20);肝动脉缝扎组(C组,n=10);假手术组(D组,n=10);部分门静脉、肝动脉同时缝扎组(E组,n=6).观察术后12周各组病死率和肝功能变化情况.免疫组化方法检测肝脏汇管区小胆管周围微血管密度、肝脏胆管增生细胞核抗原;透射电镜观察肝脏超微结构的改变.结果 术后12周肝功能检测显示,A、B、C、D组谷草转氨酶分别是(132.69±21.03)U/L、(154.40±28.73)U/L、(125.84±26.60)U/L、(134.02±18.42)U/L,各组之间差异无统计学意义(P＞0.05);谷丙转氨酶各组分别是(39.33±8.62)U/L、(44.84±9.47)U/L、(40.41±8.04)U/L、(38.47±7.29)U/L,各组之间差异无统计学意义(P＞0.05).与C、D组相比,A组和B组病死率分别为20％和25％,病死率增加,肝脏小胆管周围血管密度增加(P＜0.05);B组肝脏胆管增生细胞核抗原表达增强,平均吸光度值为0.345±0.027,较A、C、D组(平均吸光度值分别为0.264±0.015、0.258±0.022和0.249±0.021)差异均有统计学意义(P＜0.01);超微结构观察A组和B组,细胞质内可见较多脂肪颗粒聚集,线粒体可出现空泡样变.结论 肝前性门静脉高压大鼠门静脉侧支血流对肝脏生理功能的维持具有较为重要的作用;肝前性门静脉高压可使肝内胆管上皮细胞和胆管周围微血管出现轻度增生,肝细胞内发生脂肪颗粒聚集;如果肝动脉血供丧失,则这些变化会更加显著.     

猪辅助性异位部分肝移植动脉重建的方法及意义

２００１年１月～７月,我们进行了猪的同种异体辅助性异位部分肝移植（ＡＨＰＬＴ）实验,现将实验情况与供肝动脉重建有关的内容总结如下。材料与方法１．实验动物健康家猪１５头,体重２５～３５ｋｇ,雌雄不限,供受体配对移植。２．手术方式按手术模式不同分两组：Ａ组：共８头,受体肝脏保持原状,其门静脉捆扎缩窄８５％以上（直径缩窄至１／３）,肝动脉结扎;供肝（右半肝）植入受体右肝下,其肝动脉结扎,下腔静脉与受体肝下下腔静脉行端侧吻合,门静脉与受体肠系膜上静脉或门静脉行端侧吻合,胆总管与受体空肠行端侧吻合（内置Ｔ…     

一种肝前性门静脉高压症模型的制备

目的通过门静脉主干部分结扎附加3周后脾静脉缩窄及其属支结扎的方法建立犬的动物模型,观察门静脉系统变化,为该方法能否建立一种具有脾亢的门静脉高压症大动物模型提供依据。方法实验犬25只,随机分为A组(正常组,n=5)、B组(对照组,n=10)、C组(实验组,n=10)。A组仅予以剖腹探查,B组予以门静脉主干部分结扎建立模型,C组则通过门静脉主干部分结扎附加3周后脾静脉缩窄及其属支结扎的方法建立模型,建模后术前及术后每周动态观察两组动物血象的变化,B、C组在预定时间点(术后第5、第9周)分别随机选择5只动物开腹观测门静脉自由压、脾脏大小、门体侧支循环形成情况,并切取脾脏行组织病理学检查,此外,术前及术后预定时间点了解骨髓增生情况变化。结果两种方法建模后,门静脉自由压的增高明显,血常规示B组红细胞和血小板在术后3周明显低于正常值,4周后开始回升,而C组血红细胞和血小板的下降能够持续到术后第9周,且脾脏形态变化及术后脾脏组织病理学改变和骨髓增生情况证实C组较B组能够形成良好的脾功能亢进状态。结论门静脉主干部分结扎附加3周后脾静脉缩窄及其属支结扎的方法建模后门静脉系统的变化符合门静脉高压症的表现,尤其是脾亢状态合适,具有良好的科研应用价值。     

术前门静脉血流速度在门静脉高压症断流术后血栓形成中的预测价值

目的 评价术前门静脉血流速度对乙型肝炎肝硬化门静脉高压症断流术后门静脉血栓形成(PVT)中的预测价值.方法 对2007年1月至2008年7月在四川大学华西医院同一外科小组行脾切除和断流术的连续45例乙型肝炎后肝硬化门静脉高压症患者,运用彩色多普勒超声测量术前1 d门静脉直径、流速以及术后7 d有无门静脉系统血栓形成.同时计算患者术前Child-Pugh评分.术后测量去脾脏血液后的脾脏重量,检测术前1 d、术后7 d凝血酶原时间(PT)和血小板计数(PLT).并将患者分为血栓组与非血栓组、高速组与低速组,分别对上述指标进行统计学对比分析.结果 术后发生门静脉系统血栓13例(28.9%),血栓组(n=13)术前门静脉流速为(19.5±5.3)cm/s,其中12例低于25 cm/s[平均(18.4±3.8)cm/s],1例为32.3 cm/s;非血栓组(n=32)术前门静脉流速为(29.6±8.0)cm/s,两组差异有统计学意义(P<0.01).低速组(n=17)和高速组(n=28)血栓发生率分别为70.6%和3.6%,差异有统计学意义(P<0.01).分别比较两种分组的患者术前Child-Pugh评分、脾脏重量、手术前后PT和PLT,差异均无统计学意义(P>0.05).25 cm/s作为指标预测术后血栓形成的敏感性为92.3%,特异性为70.6%.结论 术前门静脉直径增加及血流速度降低是导致术后门静脉系统发生血栓的主要危险因素,尤其当门静脉流速降低(<25 cm/s)时,断流术后血栓发生率将显著增高.门静脉直径与血流速度存在负相关系,可根据门静脉流速预测门静脉高压症断流术后的血栓的形成.     

猪辅助性异位部分肝移植

目的 探讨辅助性异位部分肝移植治疗急性缺血性肝衰的效果。方法 用家猪配对行辅助性异位部分肝移植治疗急性缺血性肝衰。随机分为两组：I组，受体肝脏保持原状，肝动脉结扎，门静脉缩窄，供肝右半肝植入受体右肝下，仅建立门静脉血供，不建立动脉血供；Ⅱ组，供肝动脉和门静脉均建立血供，其它手术内容与I组相同。监测各组受体存活情况、肝功能、肝脏血流情况、病理及供肝胆汁分泌情况。结果 Ⅱ组受体成活率显著高于I组。I组术后胆红素显著高于术前，Ⅱ组手术前后胆红素无显著变化，I组术后胆红素显著高于Ⅱ组。I组供肝无或仅有少量胆汁分泌，肝细胞大片坏死；Ⅱ组供肝胆汁分泌和血供良好，肝细胞存活良好并有活跃的代偿性增生；I，Ⅱ组自体肝脏均大片坏死。结论 受体肝动脉结扎、门静脉缩窄能造成急性缺血性肝衰。辅助性异位部分肝移植可以治疗肝衰，效果良好。供肝必需建立良好的动脉血供。     

缝扎肝右静脉后肝动脉与门静脉血流改变的实验研究

目的：探讨结扎主肝静脉对肝动脉与门静脉血流动力学的影响。方法：小型猪共12头，剖腹后，电磁血流计测量结扎前后肝动脉、门静脉血流，大网膜静脉置管测量结扎前及结扎后30min、1、3、5、7、14、21、28、56d的自由门静脉压力(FPP)，56d后再次开腹测量肝动脉、门静脉血流。结果：FPP术后均升高，以术后7d内明显，6头超过35cmH2O，且其中3头小猪出现上消化道出血；肝动脉血流速早期增加，56d降至略高于术前水平；门静脉血流速早期减少，未检测到逆向血流，术后56d，门静脉血流速恢复为略低于术前水平。结论：结扎一条主肝静脉不会引起结扎肝叶的萎缩坏死，可能会导致上消化道出血。     

剥夺宿主肝部分门脉血供对异位植移肝和宿主肝的影响

异位移植肝易发生萎缩而失去其功能．认为是免疫排斥功能竞争和血供等多种因素所致。为了探索其主要因素，我们以美国的迪卡猪为实验对象，为了摒除排斥因素的作用，选用同窝猪作为供、受体，分2组进行部分异位肝移植。供肝切除左半肝，将右半肝植人受体右肝下．供肝肝上下静脉与受体肝下肾以上下腔静脉行端侧吻合。供肝动脉带一段胸主动脉与受体肾以下主动脉行端侧吻合．其中一组动物在血管重建后，缩窄受体门静脉，以剥夺宿主肝的部分血供；另一组不缩窄门静脉作为对照。实验结果表明，门脉缩窄组存活5d以上的猪，宿主肝均发生萎缩，井呈现明显的缺血外貌，而移植肝无一发生萎缩和缺血表现。未缩窄门静脉的一组动物，移植肝均发生萎缩，宿主肝无改变。结果提示，剥夺宿主肝部分门静脉血液供应，以保证异位移植肝的门脉血供是造成异位移植肝存活、宿主肝萎缩的有效措施，从而证实了异位移植肝发生萎缩的主要因素是门静脉供血问题。     

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。     

Auxiliary heterotopic partial liver transplantation in pigs with acute liver failure

Fulminant hepatic failure is usually fatal without liver transplantation; however, orthotopic liver transplantation is often difficult to perform due to the high risk of coagulopathy and the development of multiple organ failure. Auxiliary heterotopic partial liver transplantation (APLT), however, has the potential to provide an effective hepatic support system considering that the host liver is left in situ and the surgical procedure is less invasive. In this report, we describe the beneficial effects of performing 60% APLT on the hepatic function and survival of pigs with acute hepatic failure induced by hepatic artery ligation. The pigs were divided into a control group of nine animals (group 1) that had portal vein and hepatic artery ligation with a side-to-side portacaval shunt, and an APLT group of seven animals (group 2) that had portal vein and hepatic artery ligation with APLT. The two left lateral lobes of the donor liver were resected, reducing the liver weight to about 60%, and the graft was placed in the right subhepatic space. No deaths occurred intraoperatively. In group 1, eight pigs died of massive liver necrosis within 48 h and one died between 48 and 72 h (median surivival 23 h). In group 2, two pigs died within 72 h due to preservation or anesthetic problems, but five survived for more than 3 days (median survival 13.4 days), with a significant difference between the two groups (P<0.05). One animal was killed 30 days after APLT and excellent graft function was demonstrated by the synthesis of clotting factors, ammonia detoxification, and glucohomeostasis. Moreover, evidence of hepatic regeneration was found in the transplanted livers. These results indicate that APLT provides metabolic support and improves survival in animals with induced acute liver failure.     

Importance of portal flow diversion in experimental auxiliary partial orthotopic liver transplantation

BACKGROUND: Auxiliary partial orthotopic liver transplantation (APOLT) has successfully been performed in patients with noncirrhotic metabolic diseases. It remains, however, unclear if intervention in the portal venous inflow is necessary to ensure adequate portal blood flow to graft and host liver. In this experimental study we evaluate the hepatic flow during APOLT. METHODS: Left lateral/medial segmental grafts were transplanted from beagle to dalmatian dogs. Vascular structures were anastomosed end-to-end. The effect of diversion of the portal flow was studied in three groups: in the ligation group (n=3) the host portal vein was tied off, the free flow group (n=6) had random flow to both livers. In the banding group (n=11) the host portal vein was banded with a adjustable strapband to restore the pretransplantation flow distribution. RESULTS: After reperfusion the blood flow through the common portal vein decreased from 49 to 36 ml/kg/min (P<0.03) in all animals. Flow through the left portal vein decreased from 26 to 5 ml/kg/min (P<0.0001). Banding restored the flow in the left portal vein to 12 ml/kg/min, although the flow in the free-flow group remained 4 ml/kg/min. In the ligation group the total portal flow was forced toward the graft leading to the highest perfusion: 24 ml/kg/min (P<0.005). Adverse effect of this ligation was the development of portal hypertension. CONCLUSIONS: This experimental study confirms that diversion of the portal flow is necessary for adequate graft perfusion in APOLT. Banding can restore the pretransplantation flow distribution, without compromising the flow in the common portal vein.     

Native Portal Vein Embolization for Persistent Hyperoxaluria Following Kidney and Auxiliary Partial Liver Transplantation

Type 1 primary hyperoxaluria (PH1) causes renal failure, for which isolated kidney transplantation (KT) is usually unsuccessful treatment due to early oxalate stone recurrence. Although hepatectomy and liver transplantation (LT) corrects PH1 enzymatic defect, simultaneous auxiliary partial liver transplantation (APLT) and KT have been suggested as an alternative approach. APLT advantages include preservation of the donor pool and retention of native liver function in the event of liver graft loss. However, APLT relative mass may be inadequate to correct the defect. We here report the first case of native portal vein embolization (PVE) to increase APLT to native liver mass ratio (APLT/NLM‐R). Following initial combined APLT‐KT, both allografts functioned well, but oxalate plasma levels did not normalize. We postulated the inadequate APLT/NLM‐R could be corrected by trans‐hepatic native PVE. The resulting increased APLT/NLM‐R decreased serum oxalate to normal levels within 1 month following PVE. We conclude that persistently elevated oxalate levels after combined APLT‐KT for PH1 treatment, results from inadequate relative functional capacity. This can be reversed by partial native PVE to decrease portal flow to the native liver. This approach might be applicable to other scenarios where partial grafts have been transplanted to replace native liver function.     

Competition between native liver and graft in auxiliary liver transplantation in a rat model

The competition between the native and the grafted liver in heterotopic auxiliary liver transplantation (HALT) with portal vein arterialization (PVA) was investigated in a rat model. The experimental groups were: HALT with flow-regulated PVA and 70% resection of a native liver and graft (n = 32; group I) versus 70% liver resection (n = 32; group II). After HALT, the weight of the native liver increased until the sixth postoperative week (431% +/- 55% of the intraoperative weight), whereas, the graft weight was only 76% +/- 31% of the intraoperative weight at this time. In group II, liver weight increased continuously to 529% +/- 30% of the intraoperative weight after 6 weeks. On postoperative day 2, there was significantly increased proliferative hepatocellular activity in all groups. This was highest in the resected livers of group II, followed by the native livers of group I, and the grafts of group I (301 +/- 126 vs 262 +/- 97 vs 216 +/- 31 Ki-67-positive hepatocytes/10 visual fields). However, the differences between the groups were not significant. With regard to hepatocellular apoptosis, the livers were similar among all groups and at all time points, M30-positive hepatocyte counts were 相似文献   

Intraoperative hemodynamics in liver transplantation comparing orthotopic with heterotopic transplantation in the pig

The intraoperative hemodynamic changes and several graft function parameters were studied comparing orthotopic liver transplantation with auxiliary partial liver transplantation (APLT) in the pig. Thirty-one Yorkshire pigs (ca. 25 kg b.w.) were randomly allocated to OLT (n = 16) or APLT (n = 15). During the construction of portal anastomosis the median cardiac output dropped to 67% of the initial value in OLT and to 49% in APLT (P less than 0.02). Median duration of the portal flow interruption was shorter in APLT: 15 min versus 48 min in OLT (P less than 0.002). After unclamping of the aorta, the median systolic blood pressure dropped to 75 mmHg in OLT and to 90 mmHg in APLT (P less than 0.02). APLT is less time-consuming: median duration of transplantation was 128 min versus 165 min in OLT (P less than 0.002). SGOT levels were lower in APLT than in OLT (median SGOT on the first postoperative day 67 was IU/L versus 177 IU/L, P less than 0.002). It is concluded that APLT is a shorter procedure than OLT with a shorter portal flow interruption, being less offensive to the recipient.     

Intraoperative flow measurement of native liver and allograft during orthotopic liver transplantation in children

Hepatic hemodynamic changes during liver transplantation (OLT) in children have not yet been studied. We measured intraoperative portal vein flow (PVF) and hepatic arterial flow (HAF) (mL/min) in 53 children and 58 grafts during OLT. Flows were measured in the native organ and in the allograft. In the native liver, PVF and HAF are similar; after transplantation they return to the physiological situation. No flow differences were seen between whole and partial grafts. Among the 8 (14%) portal vein thromboses, PVF was lower in both the native liver and the graft than in the no thrombosis group (P < .05). PVF <5 mL/min/kg was a risk factor to develop PV thrombosis. No graft loss occurred in 3 cases without PVF at the time of OLTs despite the observation that repermeabilization was not possible. In 4 patients with PVF <5 mL/min/kg, after tying a spontaneous spleno-renal shunt (n = 3) or performing a porto-renal vein anastomosis (n = 1), PVF reached >20 mL/min/kg, avoiding thrombosis. In conclusion, PVF and HAF measurements during pediatric OLT may predict patients at high risk for development of PV thrombosis.     

Relationship between portal venous flow and liver regeneration in patients after living donor right-lobe liver transplantation

The purpose of this study is to evaluate the relationship between portal venous (PV) velocity and degree of liver regeneration in humans after living donor liver transplantation (LDLT). Between July 1997 and September 2002, a total of 15 adult-to-adult LDLTs with right-lobe grafts were performed, and 13 of these patients were enrolled in this study. Postoperative PV dynamics differed according to the primary liver disease; therefore, patients were divided into two groups: a fulminant hepatic failure (FHF) group (n = 4) and a liver cirrhosis (LC) group (n = 9). Right-lobe donors (n = 13; D group) were used as controls. Doppler ultrasound was used to measured changes in PV velocity preoperatively; postoperative days (PODs) 1, 3, 7, 14, and 28; and 3 months after LDLT. To assess hepatic regeneration, the increase in liver volume ratio (postoperative liver volume to standard liver volume [SLV]) was measured. PV velocity after LDLT in the LC group increased sharply until POD 7, whereas those in the FHF and D groups were constant. In the first 3 months after LDLT, mean PV velocity was greater in the LC group than the other groups, reflecting the persistent hyperdynamic state in chronic end-stage liver disease. Liver regeneration also was more rapid in the LC group than the FHF and D groups and reached 100% as early as 2 weeks posttransplantation, whereas both the FHF and D livers reached approximately 80% of SLV at 3 months. PV velocity POD 7 correlated significantly with regeneration of the partial-liver allograft at 1 month (r = 0.84; P = .0091). In conclusion, the PV persistent hyperdynamic state in the LC group could directly trigger early liver regeneration in partial-liver allografts after LDLT. (Liver Transpl 2003;9:547-551.)     

Excessive portal flow causes graft nonfunction in small size liver transplantation: an experimental study in pigs

We investigated the effects of portocaval shunt (PCS) on excessive portal flow in producing sinusoidal microcirculatory injury in small-for-size liver transplants in pigs. The posterior segment of a whole liver (25%) was transplanted orthotopically. The pigs were divided two groups: group A, graft with PCS (n = 11), and group B, graft without PCS (n = 11). The PCS was a side-to-side anastomosis of the portal vein and the inferior vena cava. In group A, eight pigs survived for more than 4 days; all pigs except for one died of graft nonfunction within 24 hours in group B. The portal flow after reperfusion decreased in group A, but increased about three times greater in group B than that before the operation (P < .01). In group B, destruction of the sinusoidal lining and bleeding in the periportal areas were observed after reperfusion, findings that were not recognized in group A. These results suggest that graft nonfunction after small-for-size liver transplantation may be attributable to excessive portal flow producing sinusoidal microcirculatory injury.     

Hemodynamic interaction between portal vein and hepatic artery flow in small-for-size split liver transplantation

In split-liver transplantation, the entire portal flow is redirected through relatively small-for-size grafts. It has been postulated that excessive portal blood flow leads to graft injury. In order to elucidate the mechanisms of this injury, we studied the hemodynamic interactions between portal vein- and hepatic artery flow in an experimental model in pigs. Six whole pig liver grafts were implanted in Group 1 ( n=6) and six whole liver grafts were split into right and left grafts and transplanted to Groups 2 ( n=6) and 3 ( n=6), respectively. The graft-to-recipient liver volume ratio was 1:1, 2:3 and 1:3 in Groups 1, 2 and 3, respectively. Portal vein- and hepatic artery flows were measured with an ultrasonic flow meter at 60,120 and 180 min after graft reperfusion. Portal vein pressure was also recorded at the same time intervals. Graft function was assessed at 3,6h and 12h, and morphological changes at 12h after reperfusion. Following reperfusion, portal vein flow showed an inverse relationship to graft size, while hepatic artery flow was reduced proportionately to graft size. The difference was significant among the three groups ( P<0.05). Portal vein pressure was significantly higher in group 3, compared to groups 1 and 2 ( P<0.05). Hepatic artery buffer response was significantly higher in Group 3, compared to Groups 1 and 2 in relation to pre-occlusion values ( P<0.05). Split-liver transplantation, when resulting in small-for-size grafts, is associated with portal hypertension, diminished arterial flow, and graft dysfunction. Arterial flow impairment appears to be related to increased portal vein flow.     

The effect of decreased portal blood flow on the biliary system

A disturbance in the regional portal blood flow adjacent to the dilated bile duct in the liver is often observed in patients with hepatolithiasis. The effects of this disturbed portal blood flow on the biliary system, with or without cholangitis, were therefore investigated. Young rabbits were divided into the following four groups; (1) controls that had a laparotomy only (n = 3), (2) those that had a ligation of the portal branch of the right posterior lobe (RP lobe) (PL) (n = 10), (3) those that had tubing inserted into the bile duct through the duodenal papilla (BS) (n = 10), and (4) PL + BS (n = 10). Despite marked atrophy of the RP lobe, no distinct changes were seen in the biliary systems of groups 1 or 2. In groups 3 and 4, however, infiltration of inflammatory cells and glandular proliferation in the wall of the markedly dilated extrahepatic bile duct (proliferative cholangitis (PC), characteristic to hepatolithiasis) were seen. Findings of PC were also noted in the intrahepatic bile duct of the atrophied RP lobes of these 2 groups. The incidence of PC was 20 per cent in group 3 and 60 per cent in group 4, respectively, but the PC of the intrahepatic bile ducts in group 3 was more localized than in group 4. Goblet cell metaplasia was seen in the epithelial cells of PC. Bacteriologically, bile samples were aseptic in groups 1 and 2, however, samples of bile from groups 3 and 4 were all contaminated with Escherichia coli or Streptococcus Faecalis. The biliary contents of phospholipids, total cholesterol and total bile acid were significantly decreased in groups 3 and 4, when compared with groups 1 and 2. In conclusion, a disturbance in portal blood flow, accompanied by cholangitis and segmental liver atrophy, may play an important role in the clinical course of hepatolithiasis.