胆汁转流性外引流术对恶性梗阻性黄疸血内毒素水平的影响

目的 :探讨外引流术体外转流胆汁对恶性梗阻性黄疸病人血内毒素水平的影响。方法 :对 14例肿瘤手术不能切除的恶性梗阻性黄疸病人行胆汁转流性外引流术 ,与同期施行的 15例内引流术、2 0例外引流术病人进行手术前后外周血内毒素水平比较。结果 :术前 3组内毒素水平差别无显著性意义 (P>0 .0 5 )。单纯外引流组手术后内毒素水平略高于术前 (P >0 .0 5 ) ;内引流组术后第 2天内毒素水平反而高于术前 (P <0 .0 5 ) ,第 7天、第 14天显著降低 (P <0 .0 5 ,P <0 .0 1) ;体外转流组术后内毒素水平逐渐降低 ,与内引流术组变化基本相同。结论 :胆汁转流性外引流术可降低恶性梗阻性黄疸病人外周血内毒素水平。     

Protective effect of the intravenous administration of ursodeoxycholic acid against endotoxemia in rats with obstructive jaundice

This study was undertaken to elucidate the effect of the intravenous administration of ursodeoxycholic acid (UDCA) on endotoxemia in rats with obstructive jaundice from the viewpoint of the biliary excretion of lipopolysaccharide (LPS) through hepatocytes. In rats with obstructive jaundice, fluorescein isothiocyanate-labeled LPS was administered via the portal vein and then its biliary excretion was examined. A significant increase in the LPS excretion was thus noticed in UDCA-treated rats at a dose of 0.1μmol/100g body wt. per min. In place of UDCA, sodium taurocholate at the same dose also enhanced the biliary excretion of LPS. Secondly, we also examined whether or not UDCA protects against endotoxemia. In this experiment, nonlabeled LPS was administered via the portal vein and its peripheral concentration was then measured. In UDCA-treated rats, the endotoxin concentration was significantly lower. Finally, to elucidate the effect of UDCA on Kupffer cells, serum tumor necrosis factor (TNF-α) was measured. But UDCA had no effect on the TNF-α level. These findings thus demonstrate that the intravenous administration of UDCA protects against endotoxemia by enhancing the transport of LPS across the hepatocytes from blood to bile without affecting Kupffer cells, and that this biliary excretion of LPS is dependent on bile acids.     

Endotoxemia,disturbance of coagulation,and obstructive jaundice

A prospective study of coagulation disturbances and endotoxemia in 42 patients having major pancreatic or biliary surgery was performed. Endotoxin, soluble fibrin, and fibrin degradation products were measured before and after operation in 28 patients with obstructive jaundice and in 14 nonjaundiced controls. In the control group there was one death and no unexplained fever or postoperative hemorrhage. The jaundiced group had more complications: seven deaths, nine episodes of fever, and six episodes of hemorrhage. Soluble fibrin was detected only in patients with obstructive jaundice, in whom it occurred in 38 percent before operation. Positive endotoxin assay was as common in control patients as in the jaundiced group, but in the latter endotoxin was associated (p < 0.05) with increased FDP and soluble fibrin. Patients with endotoxin or increased FDP levels before operation for jaundice carry a poor prognosis (7 of 11 died). Preoperative bowel preparation in 16 of the jaundiced patients did not affect the outcome.     

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.     

内毒素血症与梗阻性黄疸病人肾功能损害的关系

目的: 探讨梗阻性黄疸(梗黄)病人血浆内毒素(ET)水平与肾功能的关系.方法: 动态观察30例梗黄(梗黄组)手术前后血浆ET、肌酐(Cr)、尿素氮(BUN)含量及内生肌酐清除率(Ccr)变化,并与21例无黄疸病人(对照组)进行同步比较.结果: 梗黄组外周血ET水平显著升高(P<0.01),Ccr显著降低(P<0.01);门静脉血ET水平又显著高于外周血(P<0.05),术后5 d内ET水平降低不明显;术后第1天ET反而升高(P<0.05),Ccrr更趋下降(P<0.05),并伴有血Cr、BUN升高(P<0.05);5 d后随ET水平逐渐下降,Cor逐步上升,第15天ET、Ccr两项指标接近正常水平;ET与Ccr呈显著负相关(r=-0.55,P<0.05).对照组血浆ET呈低水平,Ccr在100ml/min左右,手术前后变化均不显著(P>0.05).结论: 肠源性内毒素血症是梗黄肾功能损害的重要原因,围手术期以手术后一周内最为严重.     

加味大柴胡汤加用L-精氨酸对阻黄大鼠血浆内毒素的影响

目的　探讨L 精氨酸、加味大柴胡汤及两者合用对保护阻塞性黄疸大鼠的肝功能、抑制脂质过氧化损伤、缓解内毒素血症的作用。方法　制作急性阻塞性黄疸大鼠模型 ,分为 7、14及 2 1d 3个时段 ,每个时段分为 5组 ,每组 6只大鼠。在各时相点 ,检测内毒素和NO2 -/NO3 -的含量。结果　门静脉血浆内毒素的含量 :胆管结扎 7d后 ,门静脉血浆内毒素含量BDL NS组明显高于其他组 (P <0 .0 1)。而BDL L Arg 中药组与BDL L Arg及BDL 中药组间比较差异有显著性 (P <0 .0 5 )。胆管结扎 14d ,门静脉血浆内毒素含量BDL L Arg 中药组与BDL L Arg及BDL 中药组比较差异也有显著性 (P <0 .0 5 )。但在 2 1d时段门静脉内毒素含量BDL L Arg组与BDL NS组比差异无显著性 ,而BDL 中药组及BDL L Arg 中药组门静脉内毒素含量较上述两组差异有显著性 (P <0 .0 1)。结论　在阻塞性黄疸发病早、中期 ,采用加味大柴胡汤加L Arg治疗对保护肝功能与缓解内毒素血症作用较佳     

阻塞性黄疸患者肝脏巨噬细胞功能变化的临床研究

为探讨阻塞性黄疸患者围手术期感染发生率明显增高的原因，对３６例阻塞性黄疸患者围手术期肝脏Ｋｕｐｆｆｅｒ细胞吞噬功能和血浆内毒素水平变化进行了观察，并与２０例单纯性胆囊结石患者进行比较。结果显示：胆道梗阻后Ｋｕｐｆｅｒ细胞吞噬功能降低，与对照组比较有显著性差异（Ｐ＜０．０５）；血浆内毒素含量升高，与对照组比较有高度显著性差异（Ｐ＜０．０１）。经手术胆道引流后，血浆内毒素水平则逐渐降低。随着Ｋｕｐｆｅｒ细胞吞噬功能恢复，血浆内毒素进一步降低。由此表明，胆道梗阻后Ｋｕｐｆｅｒ细胞吞噬功能变化与血浆内毒素水平有显著的相关关系。     

Circulating immune complex, endotoxin, and biliary infection in patients with biliary obstruction

Immunoglobulin A-containing circulating immune complexes, immunoglobulin G-containing circulating immune complexes, and endotoxin were measured in the sera of patients with obstructive jaundice. The bile of patients with percutaneous transhepatic biliary drainage was also cultured for bacteriologic studies. There was a significantly positive correlation between the endotoxin levels and both immunoglobulin A-containing circulating immune complex and immunoglobulin G-containing circulating immune complex. The endotoxin levels of the patients with gram-negative infections were significantly increased compared with those of the patients with sterile cultures. The immunoglobulin G-containing circulating immune complex levels of the patients with bacteria in bile were significantly increased compared with those of the patients with sterile cultures. The immunoglobulin A-containing circulating immune complex levels of the patients with bacteria in bile were slightly increased, but the difference did not reach statistical significance. These results indicate that one of the causes of increased circulating immune complex levels may be endotoxemia in combination with biliary infection in patients with biliary obstruction.     

Experimental and clinical study of lactulose in obstructive jaundice

The role of lactulose in preventing endotoxaemia in obstructive jaundice has been investigated. A prospective study was performed on 24 consecutive patients with obstructive jaundice undergoing surgery. Twelve patients were given oral lactulose before operation and were compared with twelve controls. Endotoxaemia was reduced in peroperative portal (P less than 0.05) and postoperative systemic (P less than 0.05) blood samples in the lactulose treated group, and a significant fall (P less than 0.05) occurred in the postoperative 24 h creatinine clearances in controls compared with the lactulose treated group. Results from animal experiments in which oral lactulose reduced endotoxin related mortality in obstructive jaundice (P less than 0.05), and the in vitro demonstration of a direct anti-endotoxic action of lactulose suggest that its beneficial action is due in part to an inactivation of endotoxin.     

Biliary sepsis: some peculiarities of pathogenesis]

Results of clinical study of 87 biliary sepsis patients and experimental study on 54 rats with obstructive jaundice and cholangitis are presented. Own and literary data are compared. Specific immune and portal haemodynamic changes, provoced by obstructive jaundice are main pathogenic factors defining specific course of biliary sepsis. These changes are: 1) gut bacterial and endotoxin translocation, portal endotoxaemia; 2) reduction of RES and Kupfer cell function and endotoxin break into the systemic circulation; 3) liver parenchyma ischemia and milliary abscess formation; 4) portal blood flow shunting into the general circulation additionally increasing systemic endotoxaemia. These factors determine rapid, even fulminate development of milliary abscesses of the liver and multiorganic failure. The authors suggest that etiologic and pathogenic factors, causing peculiarities of the clinical course should be indicated in the diagnosis of septic patient.     

Endotoxemia after surgery in digestive diseases

The blood level of endotoxin after operations in patients with digestive diseases, mainly liver cirrhosis and obstructive jaundice, and the complications most likely related to the presence of endotoxemia were investigated. Twenty-seven patients without either liver cirrhosis or obstructive jaundice showed a minimal elevation of the endotoxin level in blood, as shown by 6.1 +/- 3.9 pg/ml at the first postoperative day and there was only one anastomotic leakage. On the other hand, 18 patients with liver cirrhosis showed a notable and persistent endotoxemia after surgery. The cirrhotic patients who especially underwent splenectomy and hepatectomy showed marked elevations of endotoxin level at the first postoperative day, with values of 151.0 +/- 46.1 pg/ml and 101.3 +/- 36.2 pg/ml, respectively, and one of these patients died of hepatic failure. Thirteen patients with obstructive jaundice developed endotoxemia evidenced by the value of 21.6 +/- 4.8 pg/ml at the first day after surgery. Among these patients, two had gastrointestinal bleeding and one developed DIC. The markedly high and persistent levels of endotoxin in patients with liver cirrhosis or obstructive jaundice may be possibly related with the development of MOF.     

654－2对梗阻性黄疸内毒素致肾脏损害的临床干预

目的 :观察梗阻性黄疸 (梗黄 )患者内毒素 (ET)对肾功能影响以及 6 5 4 2的干预作用。方法 :30例梗黄患者 ,随机分为两组 ,分别给予一般治疗 (A组 )和 6 5 4 2治疗 (B组 ) ,观察手术前后血ET及内生肌酐清除率 (Ccr)变化 ,并与 2 1例无黄疸患者进行同步比较。结果 :(1)入院时A、B两组外周血ET及Ccr水平无显著差异 (P >0 0 5 ) ,但ET水平均显著高于对照组 (P <0 0 1) ,Ccr均显著低于对照组 (P <0 0 1)。 (2 )A组门静脉血ET水平显著高于外周血 (P <0 0 5 ) ,A组术后随ET水平下降 ,Ccr逐渐升高 ,第 15天ET和Ccr两项指标达到正常水平。ET与Ccr呈显著负相关 (r =- 0 5 9,P <0 0 5 )。 (3)B组用药后外周血和术中门静脉血ET水平均显著降低 ,术后保持较低水平 ,而Ccr用药后略有升高 ,术后继续上升 ,第 10天ET、Ccr两项指标达到正常水平。结论 :6 5 4 2可降低梗黄患者肠源性ET水平 ,对肾功能损害具有良好的保护作用。     

Experimental obstructive jaundice disrupts intestinal mucosal barrier by altering occludin expression: beneficial effect of bombesin and neurotensin

BACKGROUND: Little is known of the molecular events leading to increased intestinal permeability in obstructive jaundice. This study was undertaken to investigate the influence of experimental obstructive jaundice on the expression of the tight junction-associated protein occludin in the intestinal epithelium. STUDY DESIGN: Seventy male Wistar rats were randomly divided into five groups: I, controls; II, sham-operated; III, bile duct ligation (BDL); IV, BDL+Bombesin (BBS) (30 microg/kg/d); and V, BDL+Neurotensin (NT) (300 microg/kg/d). At the end of the experiment, on day 10, endotoxin was measured in portal and aortic blood. Tissue sections of the terminal ileum were examined histologically and immunohistochemically for evaluation of occludin expression in the intestinal epithelium. Lipid peroxidation and protein oxidation were determined on tissue homogenates from terminal ileum and microbiologic analysis was performed in cecal contents. RESULTS: Obstructive jaundice resulted in portal and aortic endotoxemia, which was significantly reduced after BBS or NT administration. In the BDL group, there was total loss of occludin expression in numerous enterocytes mainly at the upper third of the villi, while a gradient of positivity existed from crypt to tip. Occludin expression was restored to control state after treatment with BBS or NT. In addition, both peptides reduced intestinal lipid peroxidation, while BBS reduced protein oxidation as well. CONCLUSIONS: Experimental obstructive jaundice induces regional loss of occludin expression in the intestinal epithelium, which may be a key factor contributing to the disruption of the mucosal barrier. Gut regulatory peptides BBS and NT prevent this alteration, leading to lower portal and systemic endotoxemia.     

Endogenous endotoxemia in patients with liver cirrhosis —A quantitative analysis of endotoxin in portal and peripheral blood

In order to investigate the mechanism of endogenous endotoxemia (that is, endotoxemia observed in the absence of infection) in patients with liver cirrhosis, the concentration of endotoxin in the portal (PO-Et) and peripheral blood (PE-Et) from fifty three patients undergoing abdominal surgery was simultaneously measured by a quantitative endotoxin assay. The PE-Et of the patients with liver cirrhosis (19.8±20.2 pg/ml, n=23) was significantly elevated, when compared with that of the patients without liver cirrhosis (9.2±5.1 pg/ml, n=30), and was close to the normal range of PE-Et obtained from thirty healthy volunteers (7.2±4.1 pg/ml, n=30). The PO-Et was also higher in the patients with liver cirrhosis than in the patients without liver cirrhosis. Moreover, PO-Et was significantly higher than PE-Et in all the patients (p<0.05). The per cent difference in the endotoxin concentration between the portal and peripheral blood (percentage of ΔEt) was significantly decreased in the cirrhotic patients, especially in those with esophageal varices, which was well correlated with the phagocytic activity of the reticuloendothelial system (RES) determined by the clearance of iron colloid. The endogenous endotoxemia is thus likely to be due to the impaired clearance of endogenous endotoxin in portal blood, resulting from both the decreased phagocytic activity of RES in the liver and the coexisting porta-systemic bypass.     

Beneficial effects of growth hormone and insulin-like growth factor I on intestinal bacterial translocation, endotoxemia, and apoptosis in experimentally jaundiced rats

BACKGROUND: This study was undertaken to investigate the effect of growth hormone (GH) and insulin-like growth factor I (IGF-I), two well-known growth factors, on bacterial translocation, endotoxemia, enterocyte apoptosis, and intestinal and liver histology in a model of experimental obstructive jaundice in rats. STUDY DESIGN: One hundred six male Wistar rats were divided into five groups: I (n = 21), controls; II (n = 22), sham operated; III (n = 22), bile duct ligation (BDL); IV (n = 21), BDL and GH treatment; and V (n = 20), BDL and IGF-I administration. By the end of the experiment, on day 10, blood bilirubin was determined, and mesenteric lymph nodes, liver specimens, and bile from the bile duct stump were cultured. Endotoxin was measured in portal and aortic blood. Tissue samples from the terminal ileum and liver were examined histologically and apoptotic body count (ABC) in intestinal mucosa was evaluated. Mucosal DNA and protein content were also determined. RESULTS: Bilirubin increased significantly after BDL (p < 0.001). Bile from the bile duct was sterile. In group III, MLN and liver specimens were contaminated by gut origin bacteria (significant versus group I and II, p < 0.001, respectively). GH reduced significantly positive cultures (p < 0.01), and IGF-I had no effect. BDL resulted in significant increase in portal and aortic endotoxemia (p < 0.001); treatment with GH and IGF-I reduced it (p < 0.001). Mucosal DNA and protein content were reduced in animals with BDL and after treatment with GH or IGF-I; an increase to almost normal levels was noted in DNA, but not in protein. Overall the ileal architecture remained intact in all animal groups. The ABC increased after BDL. After GH and IGF-I administration, the ABC decreased significantly, and there was no difference between GH and IGF-I treated animals. After BDL, liver biopsies displayed typical changes of biliary obstruction, which were significantly improved after administration of GH and IGF-I. CONCLUSIONS: Treatment with GH and IGF-I in rats with experimental obstructive jaundice reduces endotoxemia, and it improves liver histology. Apoptosis, in the intestinal epithelium, may serve as a morphologic marker of the ileal mucosal integrity, demonstrating the proliferative potential of GH and IGF-I in cases of obstructive jaundice, and this might be of potential value in patients with such conditions.     

Endogenous endotoxemia in patients with liver cirrhosis--a quantitative analysis of endotoxin in portal and peripheral blood

In order to investigate the mechanism of endogenous endotoxemia (that is, endotoxemia observed in the absence of infection) in patients with liver cirrhosis, the concentration of endotoxin in the portal (PO-Et) and peripheral blood (PE-Et) from fifty three patients undergoing abdominal surgery was simultaneously measured by a quantitative endotoxin assay. The PE-Et of the patients with liver cirrhosis (19.8 +/- 20.2 pg/ml, n = 23) was significantly elevated, when compared with that of the patients without liver cirrhosis (9.2 +/- 5.1 pg/ml, n = 30), and was close to the normal range of PE-Et obtained from thirty healthy volunteers (7.2 +/- 4.1 pg/ml, n = 30). The PO-Et was also higher in the patients with liver cirrhosis than in the patients without liver cirrhosis. Moreover, PO-Et was significantly higher than PE-Et in all the patients (p less than 0.05). The per cent difference in the endotoxin concentration between the portal and peripheral blood (percentage of delta Et) was significantly decreased in the cirrhotic patients, especially in those with esophageal varices, which was well correlated with the phagocytic activity of the reticuloendothelial system (RES) determined by the clearance of iron colloid. The endogenous endotoxemia is thus likely to be due to the impaired clearance of endogenous endotoxin in portal blood, resulting from both the decreased phagocytic activity of RES in the liver and the coexisting porta-systemic bypass.     

Portal and peripheral endotoxins in patients with esophageal varices undergoing surgery

Under the hypothesis that portal endotoxemia, which has been considered evidence of endogenous endotoxemia, is actually a false-positive reaction of the Limulus test, the conventional method of determination, Toxicolor (TOX) and a new endotoxin-specific method, Endospecy (ES) were investigated, whereby portal endotoxemia was reexamined. Peripheral and portal blood samples were collected from 12 patients at various intervals during surgery for esophageal varices, and then evaluated by TOX and ES, the normal values of which are under 60.0 pg/ml and under 9.8 pg/ml, respectively. The mean peripheral and portal endotoxin (Et) levels by TOX were 23.1 pg/ml and 38.9 pg/ml, 1.5 h after the start of surgery, which continued to increase thereafter, the corresponding levels being 48.1 pg/ml and 58.7 pg/ml 8 h after the start of surgery, respectively. The portal Et levels were significantly higher by ES, indicating portal endotoxemia, the mean peripheral and portal Et levels being 6.9 pg/ml, and 6.5 pg/ml, 1.5 h after the start of surgery, these levels showing changes within a similar range. The levels determined by the conventional TOX method increased with time, to a portal Et level of 5.0 pg/ml 8 h after the start of surgery, whereas those determined by ES changed within the same range suggesting that the onset of portal endotoxemia primarily involves the G-factors and that endogenous endotoxemia does not occur.     

不同胆汁引流方式对梗阻性黄疸兔血清内毒素与免疫功能的影响

目的:探讨不同胆汁引流方式对梗阻性黄疸兔血清内毒素与免疫功能的影响。方法:将36只新西兰白兔随机均分为假手术组、外引流组、内引流组。外引流组与内引流组先建立可逆型梗阻性黄疸模型,7 d后解除梗阻,分别行胆汁外引流与内引流;假手术组按相同时间间隔行2次假手术。各组分别于造模前、造模后7 d、引流术后7 d采血,检测肝功能指标、血清内毒素水平、血中CD4+CD25+调节性T细胞的比例。结果:假手术组各时间点各项指标均无明显变化(均P0.05);造模后7 d,外引流组与内引流组血清胆红素、转氨酶、内毒素水平均较造模前明显升高,血CD4+CD25+调节性T细胞比例较造模前明显降低(均P0.05);行引流术7 d后,外引流组与内引流组肝功能指标、内毒素水平、CD4+CD25+调节性T细胞比例均较造模后7 d明显恢复,但内引流组后两项指标的恢复程度均明显优于外引流组(均P0.05)。结论:胆汁内引流较胆汁外引流更有利于梗阻性黄疸内毒素清除与机体免疫功能快速恢复。     

梗阻性黄疸患者的内毒素血症及其对机体的影响

４９例梗阻性黄疸（梗黄）患者（实验组）和８１例无黄疸胆系疾病患者（对照组）围手术期外周血的内毒素（ＥＴ）检测结果表明，实验组：①术前ＥＴ阳性率明显高于对照组（Ｐ＜０．００１）；②术后１０～１２天夹闭Ｔ／Ｙ管后ＥＴ阳性率明显低于术前和夹管前（Ｐ＜０．００１）；③伴急性化脓性胆管炎（ＡＣＳＴ）的患者ＥＴ阳性率明显高于无ＡＣＳＴ的患者（Ｐ＜０．００１）。作者认为，本组梗黄患者中出现的肾功能障碍、胃肠道出血以及２例患者的死亡，可能部分与内毒素血症有关。     

Preoperative internal biliary drainage is superior to external biliary drainage in liver regeneration and function after hepatectomy in obstructive jaundiced rats

OBJECTIVE: To examine the differences in regeneration rates and functions of the liver at the time of and after hepatectomy in obstructive jaundiced rats with preoperative external and internal biliary drainage. SUMMARY BACKGROUND DATA: The significance of biliary drainage before surgery is controversial in patients with obstructive jaundice. METHODS: After biliary obstruction for 7 days, rats were randomly divided into three groups: obstructive jaundice and hepatectomy (OJ-Hx), external biliary drainage and hepatectomy (ED-Hx), and internal biliary drainage and hepatectomy (ID-Hx). The OJ-Hx group underwent hepatectomy without biliary drainage; the other two groups underwent hepatectomy after biliary drainage for 7 days. At the time of hepatectomy, all rats were provided with internal biliary drainage. On days 0, 1, 2, 3, and 7 after hepatectomy, the DNA synthesis rate and the concentrations of adenine nucleotides and malondialdehyde in the liver were determined as markers of the hepatic regeneration rate, energy status, and lipoperoxide concentration, respectively. Portal endotoxin concentrations were measured and serum hyaluronic acid concentrations were determined as an indicator of hepatic endothelial function. RESULTS: The relative liver weight was significantly higher in the ID-Hx group than in the OJ-Hx group on days 1, 3, and 7 after hepatectomy and than in the ED-Hx group on days 1 and 2. The rate of hepatic DNA synthesis was significantly higher in the ID-Hx group than in the OJ-Hx and ED-Hx groups on day 1. The rate was similar in the ED-Hx and ID-Hx groups on day 2 but was significantly higher than in the OJ-Hx group. The hepatic malondialdehyde concentration was significantly higher on day 1 in the ED-Hx group than in the other two groups. It was lowest in the ID-Hx group throughout the study. Both biliary drainage procedures lowered the portal endotoxin concentration and serum hyaluronic acid concentration at the time of hepatectomy. The serum hyaluronic acid concentration was lowest in the ID Hx group. Hepatic adenine triphosphate concentrations and energy charge levels were similar among the three groups. CONCLUSION: Although both external and internal biliary drainage before hepatectomy improved serum liver function tests, portal endotoxin concentration, and serum hyaluronic acid concentration at the time of surgery, preoperative internal biliary drainage was superior to external drainage, as evidenced by the better liver regeneration and function after hepatectomy.