Experimental study of hepatic inflow occlusion in extrahepatic obstructive jaundice--effects on systemic and hepatic hemodynamics and oxygen metabolism]

The effect of clamping both the hepatic artery and portal vein for 20 min in extrahepatic obstructive jaundice on systemic and hepatic hemodynamics and oxygen metabolism were studied in dogs, and the following results was obtained. 1) Dogs with obstructive jaundice were in a hyperdynamic state before hepatic inflow occlusion, showing an increased demand for oxygen in the liver. 2) After declamping, cardiac index and systemic oxygen delivery were decreased in normal dogs, but a further decrease was found in dogs with jaundice. 3) After declamping, hepatic arterial blood flow was increased in normal dogs. Portal blood flow was decreased just after declamping, but was soon restored. In dogs with jaundice, hepatic arterial blood flow increased to a lesser extent, and recovery of portal blood flow was delayed. 4) Hepatic oxygen consumption and oxygen extraction ratio were already increased markedly just after declamping in normal dogs, whereas the degree of the increase in these parameters was much smaller in dogs with jaundice. Thus, hepatic inflow occlusion in extrahepatic obstructive jaundice induces evident disorder of hepatic oxygen metabolism, and is suggested to be dangerous.     

Hepatic arterial buffer response fails to restore hepatic oxygenation after temporary liver dearterialization in canines

BACKGROUND: Hepatic artery thrombosis is a rare but extremely troublesome condition after liver transplantation. Recently, urgent arterial revascularization has been used as rescue therapy, leading to improved graft and patient survivals. Hepatic artery ligation produces a progressive reduction in portal vein blood flow. Theoretically, a hyperemic response may be expected following hepatic artery reperfusion (hepatic artery buffer response, HABR). In this study, we tested the hypothesis that HABR can maintain adequate liver oxygenation after temporary liver dearterialization. METHODS: Seven dogs (19.7 +/- 1.2 kg) subjected to 60 minutes of hepatic artery occlusion were observed for 120 minutes thereafter. Systemic hemodynamics was evaluated through Swan-Ganz and arterial catheters, and splanchnic perfusion by portal vein and hepatic artery blood flows (PVBF and HABF) via an ultrasonic flowprobe. Liver enzymes (ALT and LDH) and systemic and hepatic oxygen delivery (DO2hepat) were calculated using standard formulae. RESULTS: Hepatic artery occlusion induced a progressive reduction in PVBF and DO2hepat. A complete restoration of HABF after hepatic artery declamping was observed; however, the DO2hepat (33.3 +/- 5.9 to 16.5 +/- 5.9 mL/min) did not return to the baseline levels. CONCLUSION: Temporary hepatic artery occlusion induced a progressive decrease in portal vein blood flow during ischemia, an effect that continued during the reperfusion period. The hepatic artery blood flow was promptly restored after declamping. However, HABR was not able to restore hepatic oxygen delivery to baseline levels during the reperfusion period.     

Experimental study on the interruption of hepatic blood flow in obstructive jaundice, with special reference to the causes of death and prolonged jaundice after biliary decompression

The purpose of this investigation was to elucidate the influence of interruption of the hepatic blood flow on survival and on prolonged jaundice after biliary decompression in dogs with obstructive jaundice. There were three experimental groups. Two or three weeks after inducing obstructive jaundice by ligation of the common bile duct with cholecystectomy, the hepatic artery (group A), portal vein (group B) or both (group C) were interrupted for various intervals, with antibiotics administration. Biliary decompression was simultaneously performed with choledochoduodenostomy. The one week survival rate after the interruption of hepatic blood flow was more than 60% at 2 and 1 hours in group A, 20 and 10 minutes in group B, 10 and 5 minutes in group C at two and three weeks after biliary obstruction, respectively. Necrosis more than 50% of the liver was observed in early death cases. Edema and stasis in the bile canaliculi were markedly observed histologically in survivors in groups A and C, accompanied with significant elevations of serum T. Bil and GPT. The changes were greater in cases with longer periods of jaundice. In obstructive jaundice, hepatic artery occlusion causes hepatic necrosis, in spite of antibiotics administration, and may induce prolonged jaundice after biliary decompression. As an indicator of the prognosis, the serum total bile acid value was useful.     

Protective effect of agiotensin II type I receptor antagonist, CV-11974, on ischemia and reperfusion injury of the liver

BACKGROUND: Microcirculatory disturbance has been shown to play a critical role in hepatic ischemia and reperfusion (I/R) injury. Angiotensin II (AngII) is one of the most potent endogenous vasoconstrictors. Angiotensin II type I (AT1) receptor antagonist has been reported to have protective effects on I/R injury of the heart and kidney. However, effect on hepatic I/R injury has not been determined. In this study, we investigate our hypothesis that AT1 receptor antagonist, CV-11974, attenuates hepatic I/R injury. METHODS: Twelve beagle dogs underwent a 2-hr total hepatic vascular exclusion with veno-venous bypass. CV-11974 was given to animals at a dose of 0.002 mg/ kg/min for 5 min followed by 0.001 mg/kg/min for 25 min via portal vein before ischemia (group II, n=6). Nontreated animals were used as the control (group I, n=6). Animal survival, hemodynamics, hepatic tissue blood flow (HTBF), liver function, platelet count, renin activity, and AngII concentration of hepatic vein, energy metabolism, and histopathology were analyzed. RESULTS: Two-week survival was 33% in group I, in contrast, 100% in group II. Mean arterial blood pressure during early reperfusion was maintained, and HTBF after reperfusion was significantly higher in group II. Treatment attenuated liver enzyme release and decrease of platelet count, increased renin and AngII, suppressed ATP degradation during ischemia and enhanced ATP resynthesis after reperfusion. Neutrophil infiltration and histopathological damages were lessened in group II. CONCLUSIONS: Our data demonstrated that the local renin-angiotensin system might play a role in hepatic microcirculation. AT1 receptor blockade with CV-11974 attenuated hepatic microcirculatory disturbance and ameliorated I/R injury.     

梗阻性黄疸SD大鼠肝热缺血再灌注损伤模型的建立

目的构建阻塞性黄疸合并肝热缺血再灌注损伤的SD大鼠模型。 方法选择SD大鼠40只随机分为4组：假手术组（Sham组）、梗阻7天组（7 d组）、梗阻14天组（14 d组）及梗阻21天组（21 d组）,每组10只。通过双重结扎并切断胆总管建立SD大鼠阻塞性黄疸模型,探索最佳梗阻时间。梗阻7 d后另择SD大鼠62只,再随机分为4组：未缺血组（0 min组,10只）、缺血15 min组（15 min组,12只）、缺血30 min组（30 min组,16只）、缺血45 min组（45 min组,24只）,分别行肝门部血管阻断0、15、30、45 min后再灌注,建立后续肝热缺血再灌注损伤模型,观察生化指标、生存率及病理学改变。 结果梗阻7 d时适合下一步建模。建立阻塞性黄疸模型后,随着肝门部血管阻断时间的延长,肝功能进行性下降,大鼠死亡率逐渐升高,各组间的差异具有统计学意义（P<0.05）;随阻断时间的延长,肝脏损害的病理学表现更为严重。其中肝门部血管阻断30 min时24 h死亡率50%,再灌注2 h后病理学上出现严重的肝细胞变性、坏死改变。 结论对于梗阻性黄疸的SD大鼠,在梗阻7 d后行肝门部血管阻断30 min再恢复血流,可有效建立梗阻性黄疸大鼠的肝缺血再灌注损伤模型。     

A case of inflammatory pseudotumor of the liver hilum successfully treated with aggressive hepatectomy

Inflammatory pseudotumor (IPT) of the liver is a rare, benign tumor. When the tumor involves the hepatic hilum, however, the clinical course of the patient becomes problematic because of obstructive jaundice and portal hypertension. Complete removal of the tumor sometimes is difficult when the hepatic hilum is extensively involved, and liver transplantation becomes necessary for such an unresectable tumor. This report concerns a 7-year-old boy who presented with obstructive jaundice and portal hypertension owing to an inflammatory pseudotumor of the hepatic hilum and was treated successfully with aggressive hepatectomy, vascular reconstructions of both the portal vein and the hepatic artery, and biliary reconstruction. The patient was discharged after 39 days of hospitalization. Eight months later, portal vein obstruction was detected and treated successfully with percutaneous transhepatic balloon dilatation of the obstructed site. The liver has continued to function well for 11 months after the tumor resection.     

The effect of antagonism of adenosine A1 receptor against ischemia and reperfusion injury of the liver

BACKGROUND: Adenosine is known to exert protective roles in hepatic ischemia and reperfusion injury, while all adenosine receptors do not play the cytoprotective roles. We have tested our hypothesis that blockage of adenosine binding to A(1) receptor by its antagonist, KW3902 [8-(noradamantan-3-yl)-1,3-dipropylxanthine] attenuates hepatic ischemia-reperfusion injury. METHODS: Adult female beagle dogs underwent a 2 h total hepatic vascular exclusion (THVE) with a venovenous bypass. Nontreated animals that underwent THVE with a venovenous bypass alone were used as the control (Group CT, n=6). KW3902 was given to the animals by continuous intraportal infusion for 60 min before ischemia at a dose of 1 microg/kg/min (Group KW, n=6). Two wk survival, hemodynamics, hepatic tissue blood flow (HTBF), liver function, energy metabolism, cAMP concentration, and histopathological findings were studied. RESULTS: Two wk animal survival was significantly improved in group KW compared with that in group CT (group CT: 16.7% versus group KW: 83.3%). HTBF, liver function, and hepatic adenine nucleotide concentration were remarkably better in group KW than group CT. In addition, cAMP concentration in group KW was maintained significantly higher than group CT. Histopathological examination revealed preservation of hepatic architecture and suppression of neutrophil infiltration into hepatic tissue in group KW. CONCLUSION: Administration of adenosine A(1) receptor antagonist before ischemia attenuates hepatic ischemia-reperfusion injury. To elicit the beneficial effect of adenosine against ischemia and reperfusion injury of the liver, it is important to oppose adenosine A1 receptor activation.     

Experimental evaluation of the effects of the intraportal administration of cyclic guanosine monophosphate on ischemia/reperfusion in the porcine liver

This study was done to examine the protective effects of cyclic guanosine monophosphate (cGMP), a second messenger of nitric oxide, for ischemia/reperfusion injury of the liver, since it is known to induce vasodilatation and to inhibit platelet aggregation. Using an experimental model of porcine liver ischemia, 8-bromoguanosine 3′,5′ monophosphate, a cGMP analog, was continuously administered into the portal vein before ischemia and after reperfusion 30 min for each in the cGMP group (n=6). Saline water was administered in the same way in the control group (n=6). The cardiac output (CO), mean arterial blood pressure (MAP), portal venous flow (PVF), hepatic arterial flow (HAF), hepatic tissue blood flow (HTBF), and hepatic tissue cGMP level were determined. Hepatic enzymes and the bile discharge were also assessed as indicators of hepatic function. The hepatic tissue cGMP level was significantly higher, and PVF, HTBF, and the bile discharge were significantly greater in the cGMP group, while there were no remarkable differences between the groups with CO, MAP, HAF, and hepatic enzymes. In conclusion, the continuous supplementation of cGMP into the portal vein was found to be beneficial for preserving both the hepatic circulation and, consequently, the hepatic function of after warm ischemia of porcine liver.     

Continuous or intermittent vascular clamping during hemihepatectomy in pigs: hyaluronic acid kinetics in the assessment of early microvascular liver damage.

OBJECTIVE: To assess the uptake of hyaluronic acid (HA) as a marker of microvascular damage in a model of hemihepatectomy in pigs having continuous or intermittent vascular inflow occlusion. DESIGN: Prospective, animal study. SETTING: Laboratory for experimental surgery, University hospital, The Netherlands. INTERVENTIONS: Total liver ischaemia was achieved during 90 minutes by continuous (n = 5) or intermittent (n = 5) occlusion of the portal vein and hepatic artery followed by 120 minutes of reperfusion. In a second series of pigs (n = 8) a left hemihepatectomy was added to the protocol. MAIN OUTCOME MEASURES: Uptake of exogenous HA was assessed before ischaemia and after 120 minutes of reperfusion, together with the galactose elimination capacity. Plasma activities of aspartate aminotransferase (AST), alanine amino transferase, and lactate dehydrogenase were measured and specimens of liver were obtained for histopathological examination. RESULTS: HA uptake was slightly reduced after reperfusion in unresected livers compared with uptake before ischaemia. After hemihepatectomy HA uptake after reperfusion was significantly reduced after both continuous and intermittent occlusion, but more HA was taken up after continuous occlusion (p = 0.02). Release of AST after reperfusion was increased only after hemihepatectomy. CONCLUSIONS: Microvascular damage, as assessed by HA uptake capacity, significantly contributed to normothermic ischaemia and reperfusion injury in porcine liver. Vascular inflow occlusion during 90 minutes in combination with hemihepatectomy resulted in less liver damage when vascular occlusion was continuous rather than intermittent.     

Hepatocellular Glycogen in Alleviation of Liver Ischemia-Reperfusion Injury During Partial Hepatectomy

Background Temporary occlusion of liver blood supply for complex liver operation is common in liver surgery. However, hepatic vascular occlusion will undoubtedly impair liver function. This study was designed to elucidate the effect of hepatocellular glycogen in alleviation of liver ischemia-reperfusion injury during hepatic vascular occlusion for partial hepatectomy. Methods Fifty-seven patients were randomly divided into an experimental group (n = 29) and a control group (n = 28). In the experimental group, patients were given high-concentration glucose intravenously during 24 h before the operation. The hepatic lesion was resected after portal triad clamping in the two groups. Noncancer liver tissue was biopsied to measure hepatic tissue ATP content and change of malondialdehyde (MDA) and superoxide dismutase (SOD). Liver function of all patients was assessed by using an automatic biochemical analysis apparatus before the operation and the first and fifth days after operation. Results The mean hepatic vascular occlusion time in the experimental group was 19.21 ± 4.54 min and in the control group it was 21.04 ± 5.11 min. Hepatic tissue ATP content of the experimental group was significantly higher than that of the control group at the end of hepatic vascular occlusion (2.15 ± 0.39 μmol/g wet tissue vs. 1.33 ± 0.44, p < 0.01) and at the point of 1-h reperfusion (2.19 ± 0.29 μmol/g wet tissue vs. 1.57 ± 0.35, p < 0.01). There was significant difference in SOD activity between the two groups at the end of hepatic vascular occlusion (130.69 ± 30.49 NU/mg pr vs. 97.83 ± 26.23, p < 0.01) and at the point of 1-h reperfusion (139.55 ± 39.88 NU/mg pr vs. 114.74 ± 25.93, p < 0.01). Significant difference was shown in MDA content between the two groups at the end of hepatic vascular occlusion (3.02 ± 0.30 nmol/mg pr vs. 3.99 ± 0.49, p < 0.01) and at the point of 1-h reperfusion (3.81 ± 0.69 nmol/mg pr vs. 5.75 ± 1.17, p < 0.01). In addition, the liver function of the experimental group was significantly better than that of the control group the first and fifth days after the operation (p < 0.01). Conclusions Abundant intracellular glycogen may reduce liver ischemia-reperfusion injury caused by hepatic vascular occlusion. It is beneficial to give a large amount of glucose before a complex liver operation during which temporary occlusion of hepatic blood flow is necessary.     

异丙酚对肝叶切除术患者肝缺血再灌注损伤的影响

目的 探讨异丙酚对肝叶切除术患者肝缺血再灌注损伤的影响.方法 拟行肝叶切除术的肝癌患者60例,年龄28～64岁,体重50～77 kg,ASA Ⅰ～Ⅲ级,随机分为对照组(Ⅰ组)和异丙酚组(Ⅱ组),每组30例.Ⅱ组肝门开放后静脉输注异丙酚4～6 mg·kg-1·h-1至术毕.分别于麻醉前(T1)、肝门阻断前(T2)、肝门阻断后15 min(T3)、肝门开放后10 min(T4)和45 min(T5)时抽取中心静脉血测定血清谷草转氨酶(AST)、谷丙转氨酶(ALT)、超氧化物歧化酶(SOD)活性,丙二醛(MDA)浓度.结果 与T1时比较,两组T3-5时AST、ALT活性升高,Ⅰ组T4,5时SOD活性降低、MDA浓度升高,Ⅱ组T4,5时SOD活性升高、MDA浓度降低(P<0.05);与Ⅰ组比较,Ⅱ组T4,5时AST、ALT活性降低,SOD活性升高、MDA浓度降低(P<0.05).结论 肝门开放后至术毕静脉输注异丙酚4～6mg·kg-1·h-1可减轻肝叶切除术患者肝缺血再灌注损伤.     

肝动脉缺血对犬肝细胞损害的实验研究

摘要：目的:探讨肝动脉缺血对犬肝细胞的损害。方法:对２０只犬进行肝动脉阻断，不阻断门静脉，分别于阻断前、阻断后２０，４０，６０min取肝组织进行活检，用常规ＨＥ染色和ＢＣＬ-２免疫组化染色并进行灰度测定。结果:肝动脉阻断２０min，肝细胞已有明显损害，阻断６０min有不可逆性严重损害，ＢＣＬ-２免疫组化灰度测定，阻断前与阻断后各时点差异均有高度显著性（P<0.0001），其中２０min和４０min与６０min之间差异有高度显著性(P<0.001)。结论:肝动脉阻断20min，肝细胞有明显损害，肝动脉阻断60 min，肝细胞有不可逆性损害。     

Lesion progression with time and the effect of vascular occlusion following radiofrequency ablation of the liver

BACKGROUND: The effectiveness of radiofrequency ablation (RFA) under selective vascular occlusion and its effects on architecture and viability of normal liver parenchyma was studied in a porcine model. METHODS: RFA was applied in the liver under general anaesthesia in 18 pigs. Six animals were killed immediately after the procedure and 12 at 24 h. RFA was performed sequentially under four conditions: (1) without vascular occlusion, (2) during occlusion of the hepatic artery, (3) during occlusion of the portal vein and (4) during occlusion of the hepatic artery and portal vein. Liver biopsies from the treated area were stained for conventional histological examination, reduced nicotinamide adenine dinucleotide diaphorase and 5'-nucleotidase activity. RESULTS: Vascular occlusion significantly increased the size of the coagulation centre after RFA. Combined portal venous and arterial occlusion had no additional effect on lesion size compared with venous or arterial occlusion alone. After 24 h, deterioration of viability was observed in the parenchyma up to 3 cm from the coagulated area. CONCLUSION: The efficacy of RFA in liver increases with occlusion of the portal vein or hepatic artery. The extent of secondary heat-induced necrosis in liver parenchyma should be considered for determination of the final size of the ablated area.     

The effect of intraportal prostaglandin E1 on adhesion molecule expression, inflammatory modulator function, and histology in canine hepatic ischemia/reperfusion injury

BACKGROUND: Prostaglandin E1 (PGE1) is known to protect the liver from I/R, however, the mechanism of cytoprotection is not well understood. This study investigates the effect of intraportal infusion of PGE1 in a warm liver ischemia/reperfusion (I/R) model on cytokines, adhesion molecules and liver structure. MATERIALS AND METHODS: Twenty dogs underwent laparotomy under general anesthesia. PGE1 (0.02 microg\kg\min) was perfused through the portal vein in the PGE1 group (n = 10), or a similar volume of Ringer's solution in the control group (n = 10) for 15 min. Liver ischemia was induced by hepatic artery and portal vein occlusion and PGE1 was infused via the portal vein for 60 min. The occlusion was released and PGE1 infusion recommenced for 30 min. Blood and liver biopsies were sampled at baseline, 60 min ischemia, and 30 min reperfusion and assessed for transaminases, cytokines, adhesion molecules, and electron microscopy. RESULTS: PGE1 infusion significantly reduced transaminases TNF-alpha, sICAM-1, sP-selectin, and sE-selectin on ischemia and reperfusion. PGE1 reduced hepatocytic degeneration, portal and central ICAM-1 expression, central and sinusoidal VCAM-1 expression, portal and central P-selectin expression, and portal and sinusoidal E-selectin expression on reperfusion. CONCLUSION: Intraportal PGE1 infusion reduced I/R injury and was associated with down-regulation of ICAM-1, VCAM-1, P-selectin, and E-selectin on reperfusion.     

Major resections of the liver in patients with high surgical risk

Experience with 75 major anatomic resections of the liver in patients with high surgical risk due to low functional reserve of the liver, spontaneous disruption of hepatic tumor, chronic purulent infection in patients with hepatic abscesses, posttraumatic sequestration of the liver with hemobilia, giant hepatic hemangiomas, old age and severe concomitant diseases was analyzed. General postoperative lethality was 14.7% which was determined mainly by unfavorable outcomes in postoperative patients in spontaneous disruption of tumor and massive intraabdominal bleeding, and also by severe postoperative hepatic insufficiency in patients after right-sided hemihepatectomy for hepatocellular carcinoma with postnecrotic cirrhosis of the liver. Immediate results of surgery in patients with obstructive jaundice and biliary hepatic cirrhosis were better that ones of patients with postnecrotic cirrhosis. There were no lethal outcomes in group of patients after surgery for giant hemangiomas, abscesses and posttraumatic sequestration of the liver. Thorough selection of patients based on detailed study of functional hepatic reserves and also volume of removed hepatic parenchyma is necessary for improvement of immediate results of surgical treatment. It is valid to perform portal venous embolization before right-sided hemihepatectomy in patients with postnecrotic, biliary cirrhosis, and also in old patients to decrease the risk of postresection hepatic insufficiency. Roentgenondovascular occlusion of the hepatic artery, Cell-Seiver use for intraoperative blood reinfusion and in some cases--use of methods of complete vascular isolation of the liver are indicated for patients with giant hepatic hemangiomas.     

Effects of biliary obstruction on hepatic clearance of bacteria

High surgical mortality in patients with obstructive jaundice and sepsis have been attributed to reticuloendothelial system (RES) depression. The purpose of this study was to clarify the effects of mechanical biliary obstruction on RES clearance of pathogenic bacteria by comparing the phagocytic index (K) with the directly measured hepatic uptake of indium 111-labeled bacteria injected into the portal vein of normal dogs and dogs with partial (PBO) or complete biliary obstruction (CBO). No significant difference was observed between the K in normal dogs (0.19 +/- 0.08; n = 6) and that in dogs with PBO (0.24 +/- 0.06; n = 5) or CBO (0.21 +/- 0.03; n = 4). There was no significant difference in uptake of radiolabel by the liver among the three groups of dogs. In our model, biliary obstruction had no effect on hepatic RES function and may not represent a significant determinant of mortality in patients with obstructive jaundice.     

N-乙酰半胱氨酸预处理对肝脏缺血再灌注损伤的保护作用

目的 探讨N-乙酰半胱氨酸(N-acetylcysteine,NAC)预处理对肝脏缺血再灌注损伤的保护作用.方法 18 例肝血管瘤手术患者随机分为3 组(n=6):对照组(C0)、NAC 预处理组(PR)和NAC 后处理组(PO),其中PR和PO 组分别于肝门阻断前和开放后给予NAC 120 mg/kg.三组患者均于切皮前(T0)、肝门阻断开放后1 h(T1)及6 h(T2)抽血检测谷丙转氨酶活性(ALT)和谷草转氨酶(AST)水平,并于肝门阻断开放后1 h(T1)取肝组织测定丙二醛(MDA)含量及核因子κB(NF-κB)活性.结果 肝门阻断开放后1 h(T1)和6 h(T6),各组的ALT 和AST 水平均明显高于肝门阻断前(T0)水平(P<0.01);与对照组相比,PR 和PO 组的MDA 含量在肝门阻断开放后1 h(T1)明显减少(P<0.01),但NF-κB 的活性仅在PR 组显示有明显的降低(P<0.01).结论 NAC 预处理可有效防治肝脏缺血再灌注损伤,其机制与抑制再灌注后NF-κB 的启动激活有关.     

Increased sinusoidal pressure is associated with early liver weight gain in ischemia-reperfusion injury in isolated perfused rat liver

BACKGROUND: Hepatic ischemia-reperfusion (I/R) is accompanied by liver weight gain and ascites formation. This could be caused by an increase in sinusoidal pressure, a determinant of hepatic transvascular fluid movement. We determined the role of sinusoidal pressure, assessed by triple vascular occlusion pressure (P(to)), in the I/R injury in isolated rat livers perfused with leukocyte-free diluted blood bivascularly via the portal vein and hepatic artery. MATERIALS AND METHODS: Ischemia was induced at room temperature by occlusion of either the inflow lines of the hepatic artery and portal vein (the open outflow group, n = 10) or both the inflow and the outflow (hepatic venous) lines (the closed outflow group, n = 10) for 1 h, followed by 1-h reperfusion in a recirculating manner. RESULTS: Liver weight in both groups increased biphasically after reperfusion; the initial peak occurred at 3 min and the second peak at 60 min. Immediately after reperfusion, P(to) peaked, followed by a gradual decline. The initial weight increase in groups combined was significantly and positively correlated with an increase in P(to) (r = 0.716, P = 0.0002), but the second peak was independent of P(to). Liver injury, assessed by perfusate levels of hepatic enzymes and reduced bile flow rate, was observed at 60 min after reperfusion in both groups. CONCLUSIONS: These findings suggest that increased sinusoidal pressure contributes to only the early liver weight gain after reperfusion in isolated perfused rat livers. The late weight gain may be presumably due to liver injury.     

Intrahepatic Segmental Portal Vein Thrombosis After Living-Related Donor Liver Transplantation

Background

Intrahepatic segmental portal vein thrombosis after living-related liver transplantation (LRLT) is uncommon. The cause remains unclear.

Methods

After providing written informed consent, 25 recipients receiving LRLT at our institution from January 2011 to September 2013 were enrolled in this study. We performed triphase computerized tomographic (CT) study of the liver graft of each recipient 1 month after LRLT. The patencies of hepatic artery, portal vein, and hepatic vein were evaluated in detail. The triphase CT scans of the liver of each donor before transplantation also were reviewed. Thrombosis of the intrahepatic segmental portal vein was defined as the occlusion site of the portal vein being intrahepatic. Extrahepatic portal vein thrombosis was excluded in this study.

Results

Among the 25 patients, 2 (8%) developed thrombosis of intrahepatic segmental portal vein. One 47-year-old man received LRLT for hepatitis B viral infection–related liver cirrhosis (Child-Pugh class C) with 3 hepatocellular carcinomas (total tumor volume <8 cm). Another 53-year-old man received LRLT for alcoholic liver cirrhosis (Child-Pugh class C). Both had developed progressive jaundice and cholangitis 1 month after surgery. Intrahepatic biliary stricture was found on the follow-up magnetic resonance images. However, liver triphase CT study demonstrated occlusion of intrahepatic portal vein of segment 8 in each patient. Radiologic interventions and balloon dilatation therapy via percutaneous transhepatic biliary drainage route improved the symptoms and signs of cholangitis and obstructive jaundice for both.

Conclusions

Thrombosis of intrahepatic segmental portal vein is not common but is usually associated with complications of intrahepatic bile duct. Early detection is important, and follow-up CT study of liver is suggested.     

Vascular occlusion techniques during liver resection

Control of bleeding from the transected liver basically consists of vascular inflow occlusion and control of hepatic venous backflow from the caval vein. Central venous pressure determines the pressure in the hepatic veins and is an extremely important factor in controlling blood loss through venous backflow. Vascular inflow occlusion (Pringle maneuver) involves clamping of the portal vein and the hepatic artery in the hepatic pedicle and gives rise to postischemic, reperfusion injury. Several strategies have been devised to reduce reperfusion injury (pharmacological interventions) or to increase ischemic tolerance of the liver (ischemic preconditioning). Intermittent clamping is recommended in complex liver resections or in patients with diseased livers. The combination of occlusion of vascular inflow and outflow of the liver results in total hepatic vascular exclusion (THVE) and is mainly used in tumors invading the caval vein. During THVE the liver can be cooled by hypothermic perfusion allowing for extended ischemia times. Selective THVE entails clamping of the main hepatic veins in their extrahepatic course, thus preserving caval flow. Safe liver surgery requires knowledge of the regular techniques of vascular occlusion for 'on demand' use when necessitated to reduce blood loss.