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At least 19 recordsLinked to original sources
PubMed1993

Regulation of bicarbonate-dependent ductular bile secretion assessed by lumenal micropuncture of isolated rodent intrahepatic bile ducts.

While intrahepatic bile duct epithelial cells secrete bile through transport of ions and water, the physiological mechanisms regulating ductular bile secretion are obscure, in part because of the lack of suitable experimental models. We report here the successful micropuncture of the lumen of isolated intrahepatic bile ducts and direct measurements of ductular ion secretion. Intact, polarized bile duct units (BDUs) were isolated from livers of normal rats by enzymatic digestion and microdissection. BDUs were cultured and mounted on a microscope in bicarbonate-containing buffer, and the lumens were microinjected with 2',7'-bis(2-carboxyethyl)-5-(and -6)carboxyfluorescein (BCECF)-dextran. Lumenal pH was measured by ratio imaging of BCECF fluorescence using digitized video fluorescent microscopy. After 36 hr in culture, the ends of BDUs sealed, forming closed compartments. After lumenal microinjection of BCECF-dextran, fluorescence was stable at the pH-insensitive wavelength, indicating no dye leakage. Serial changes in pH of extralumenal buffers containing pH-gradient collapsing ionophores allowed us to establish reliable standard curves relating fluorescence ratio to lumenal pH (r = 0.99; P < 0.001). By this approach, the basal pH inside the lumen of BDUs was 7.87 +/- 0.08 units (n = 9), 0.47 unit higher (P < 0.001) than the bathing buffer pH. Addition of 100 microM forskolin increased (P = 0.02) the lumenal pH from 7.78 +/- 0.06 to 7.97 +/- 0.06 units (n = 5); the forskolin effect was completely abolished by incubation of BDUs in HCO3-/CO2-free buffer. Moreover, forskolin caused a 50-fold increase in cAMP levels in BDUs. The observations are consistent with cAMP-dependent, active lumenal HCO3- secretion by BDUs. Furthermore, they demonstrate the suitability of the BDU model for studying regulatory and mechanistic aspects of ductular bile secretion.

Analysis of Variance↗
PubMed1993

Expression of alpha-amylase isoenzymes and trypsin by the proliferating epithelium of large intrahepatic bile ducts and intrahepatic peribiliary glands in hepatolithiasis.

The expression of alpha-amylase isoenzymes (pancreatic and salivary) and trypsin by the epithelium of large intrahepatic bile ducts and peribiliary glands was examined immunohistochemically in hepatolithiasis (n = 22), extrahepatic biliary obstruction (n = 20) and normal liver (n = 22). Hepatolithiasis was associated with marked proliferation of bile duct cells and peribiliary glands. Expression of pancreatic and salivary amylase was observed in the proliferating bile duct cells and peribiliary glands of all livers, and trypsin was found in 68% of the livers. In extrahepatic biliary obstruction, proliferation of the biliary epithelium was less marked, but expression of amylase isoenzymes was observed in all livers and trypsin was found in 50%. All normal livers showed expression of amylase isoenzymes in large intrahepatic bile ducts, septal bile ducts and peribiliary glands, and trypsin was found in 73%. The density of enzyme-containing acini was highest in hepatolithiasis, intermediate in extrahepatic biliary obstruction and lowest in normal liver. These results show that the proliferating biliary epithelium in hepatolithiasis contains amylase isoenzymes and trypsin and that biliary epithelium retains the ability to produce these enzymes after proliferation, suggesting that a large amount of amylase isoenzyme and trypsin may be secreted into the bile ducts in hepatolithiasis. These enzymes may play an important role in the pathophysiology of hepatolithiasis.

Adult↗
PubMed1985

Changes of intrahepatic bile duct dilatation after surgery for congenital dilatation of the bile duct.

Of 47 patients suffering from congenital dilatation of the bile duct whose intrahepatic bile ducts could be clearly demonstrated by operative cholangiogram or preoperative ERCP, 39 patients (83%) had dilatation of the intrahepatic bile ducts. Follow-up studies in infants and children ranging from 1 year to 11 years after their corrective operation for congenital dilatation of the common bile duct showed no morbidity that was attributed to the presence of the dilatation of the intrahepatic bile ducts. ECHO grams in 21 patients revealed marked decrease in size of the intrahepatic bile ducts except for two patients with huge cystic dilatation of the intrahepatic bile ducts. These findings justify the employment of the standard operative procedure for the treatment of congenital dilatation of the bile duct even if it is associated with dilatation of the intrahepatic bile ducts.

Adolescent↗
PubMed1988

[A case of duplication of the common bile duct with anomaly of the intrahepatic bile duct].

A 50-year-old man, with a complaint of fever and epigastralgia, was admitted to the Yamaga City Hospital. Choledocholithiasis and stenosis of the lower part of choledochus were pointed out. Cholecystectomy, choledocholithotomy and papilloplasty were performed and the choledochotomy closed over a T-tube. T-tube cholangiograms, after operation, revealed stenosis, negative shadow and abnormal branching of the left intrahepatic bile duct. Then, the lateral segmentectomy of the liver was done. But the negative shadow didn't disappear . With further examination, we could find the accessory bile duct in the retroperitoneal space. Cholangiogram, from this accessory bile duct, revealed patency of this bile duct into the left intrahepatic bile duct and the duodenum. A final diagnosis of duplication of the common bile duct was established. We collected Japanese cases of this anomaly and discussed a classification of the disorder.

Abnormalities, Multiple↗
PubMed1986

A light and electron microscopic study of the regenerative epithelium in the intrahepatic bile duct. Experimental study of local direct instillation of paraquat into the intrahepatic bile ducts of rats.

To date, no reliable report on the regeneration of the intrahepatic bile duct epithelium following damage to the duct has been published. In this study, a direct instillation of paraquat dichloride into the intrahepatic bile ducts of rats was carried out, and the livers were examined under light and electron microscopy. One hour after treatment, the biliary epithelia showed degeneration and necrosis, and these changes remained for a considerable period in a large majority of the ducts examined. Three weeks after instillation, low columnar epithelium consisting of hyperchromatic nuclei and eosinophilic cytoplasm was present in a medium-sized bile duct, which was collared by marked periductal fibrosis. Electron microscopically, the eosinophilic epithelium showed a marked increase in the number of rough endoplasmic reticula, ribosomes, mitochondria, and filamentous structures, suggesting an active viability of the cell. Subsequently, the eosinophilic cells were replaced by normal-appearing epithelium, not associated with the periductal fibrosis. The data suggest that an epithelial regeneration occurred in the intrahepatic duct following injury and that this activity may be similar to that of the extrahepatic bile duct epithelium.

Animals↗
PubMed1991

Immunohistochemical demonstration of pancreatic alpha-amylase and trypsin in intrahepatic bile ducts and peribiliary glands.

Epithelia of intrahepatic bile ducts and peribiliary glands were immunohistochemically examined for pancreatic alpha-amylase and trypsin in 54 normal autopsied livers. alpha-Amylase was evaluated with a polyclonal antibody, and trypsin was assayed with both polyclonal and monoclonal antibodies. alpha-Amylase was observed in large ducts, septal ducts and peribiliary glands in most livers and was seen in interlobular ducts in seven (13%) livers. Trypsin immunoreactivity with the polyclonal antibody was observed in peribiliary glands in 21 (39%) livers; it was absent in intrahepatic bile ducts in all but one liver. Trypsin immunoreactivity with the monoclonal antibody was present in large ducts, septal ducts and peribiliary glands in about 70% of the livers and was seen in interlobular ducts in two (4%) livers. Bile ductules were always negative for the two antigens. Some epithelia of peribiliary glands positive for both alpha-amylase and trypsin histologically resembled pancreatic acinar cells. alpha-Amylase and trypsin immunoreactivities of intrahepatic biliary epithelia and pancreatic aninar cells were eliminated by absorption of primary antibodies by alpha-amylase or trypsin, suggesting the specificities of the immunoreactivities. These data suggest that epithelia of intrahepatic large ducts, septal ducts and peribiliary glands contain pancreatic alpha-amylase in most livers and that they contain trypsin in about 70% of livers. alpha-Amylase and trypsin may be secreted into intrahepatic bile duct lumens, thereby exerting important effects on the physiology of the intrahepatic biliary tree and hepatic bile.

Adult↗
PubMed1996

Intrahepatic bile duct stenosis causing intrahepatic calculi formation following excision of a choledochal cyst.

BACKGROUND: Formation of intrahepatic calculi is one of the major late complications after excision of a choledochal cyst. There are few studies, however, that have examined this complication. Generally, an anastomotic stricture is believed to be the main cause of intrahepatic calculi. We report our experience with eight patients who had intrahepatic calculi after excision of a choledochal cyst. STUDY DESIGN: To determine what caused the intrahepatic calculi to form, seven patients underwent cholangioscopy and direct visual inspection during the operation, and one patient underwent percutaneous transhepatic cholangioscopy. Intrahepatic bile was cultured, and calculi were analyzed. RESULTS: Two types of stenoses (membranous and septal) were demonstrated near the hepatic hilum in all patients. Calculi were always located on the hepatic side of the stenoses. No anastomotic strictures were found in the region of the hepaticojejunostomy. The calculi contained mainly calcium bilirubinate. Escherichia coli and Klebsiella pneumoniae were cultured from the bile in all patients. CONCLUSIONS: Stenoses of the intrahepatic bile ducts were demonstrated in all eight patients. The stenoses were considered to be the primary cause of intrahepatic calculi formation after excision of the choledochal cysts.

Adolescent↗
PubMed1995

Increased turnover of intrahepatic bile ducts induced by bromobenzene.

Intrahepatic bile duct epithelium consists of two kinetic compartments: a progenitor (P) and a functional (Q) compartment. Hitherto bromobenzene was known to poison only hepatocytes in the third acinus zone. The present experiment aims to demonstrate that bromobenzene affects also bile duct turnover. Thirty male adult rats received one intraperitoneal injection of bromobenzene and were sacrificed in groups of five at the following times: 1, 2, 3, 4, 7, and 14 days. They received [3H]thymidine 1 hr before sacrificing. Autoradiography was done. Bile ducts were evaluated in all portal tracts of the section. The number of epithelial cells in each duct cross section was counted and defined as bile duct class, which is roughly proportional to bile duct size. In each cross section the number of labeled cells was counted. Initially the labeling index was 0.76 +/- 0.3%. By day 3, it reached a peak of 4.1 +/- 1.1%, and then declined to its initial level. Following bromobenzene poisoning, hepatocyte and bile duct epithelia turn over in the same fashion. In both, labeling index and progenitor compartment size initially rise and return by the end of the first week to their initial level. We propose that bile duct epithelia and hepatocytes originate in one determined uncommitted stem cell that resides in the Herring duct. Bromobenzene-induced necrosis triggers proliferation of progenitors in both cell lineages, as well as in the stem cell itself.

Animals↗
PubMed1987

The syndrome of disappearing intrahepatic bile ducts.

Diseases with disappearing intrahepatic bile ducts may be developmental, immunological, infective, vascular, or chemical in origin. The immunological group includes primary biliary cirrhosis, graft-versus-host disease, and sarcoidosis. HLA class 2 antigens are displayed on the bileducts and recognition of biliary antigens by cytotoxic T-cells leads to destruction of interlobular ducts. Primary sclerosing cholangitis is associated with immunological features, but the hepatic histology is not that of immunological duct disease. The association with immunodeficiency syndromes, and the finding that secondary sclerosing cholangitis may occur in patients with the acquired immunodeficiency syndrome who are infected with cytomegalovirus, suggest that primary sclerosing cholangitis might be infective in origin. In bacterial cholangitis there is contiguity between the biliary system and the intestinal tract and usually, but not necessarily, partial biliary obstruction. Interference with the hepatic arterial supply to the bileducts leads to vascular cholangitis. Chemical cholangitis follows injection of scolicidal agents into the biliary tree. Diseases with disappearing bileducts have a long natural history and hepatocellular failure occurs late. In the late stages hepatic transplantation gives good results.

Bacterial Infections↗
PubMed1977

Malignant papillomatosis of the intrahepatic bile ducts.

A case of intrahepatic bile duct papillomatosis is reported which recurred several times and finally progressed into a mucin-secreting papillary adenocarcinoma. The paillomatosis predominantly involved the ductal system of the left hypoplastic hepatic lobe. The treatment consisted of a left partial hepatectomy. Hereby, a four-year survival was reached. While the prognosis of solitary papillomas in the distal choledochus and in the gallbladder is considered as good, the prognosis of the intra- and extrahepatic bile duct papillomatosis appears unfavorable. The experience in this case, as well as in the literature, shows that these papillomatoses have to be regarded as low-grade carcinomas.

Adult↗
PubMedDate not supplied

Preoperatively undiagnosable intrahepatic bile duct dilatation contains early-stage intrahepatic cholangiocarcinoma.

Intrahepatic bile duct dilatation is a clue to indicating the presence of IHCC. Moreover it is still often difficult to find IHCC at an early stage in spite of recent progress in the area of molecular biological markers and imaging modalities. We had three interesting cases in which we were suspicious of the presence of IHCC. Preoperative imaging studies of these three cases showed the dilatation and stenosis of the intrahepatic bile duct without any apparent mass. As IHCC could not be ruled out, a hepatectomy was done for the purpose of both diagnosis and treatment of the patients. Postoperative diagnoses were IHCC in one, hepatolithiasis in another and chronic cholangitis in the third patient. A histological analysis revealed that the tumor of IHCC was not infiltrating the parenchyma of the liver with neither vascular nor lymphatic invasion, which suggested that it was an initial nature of the IHCC. In the case of intrahepatic bile duct dilatation and stenosis, which makes it hard to identify IHCC, surgical resection is crucial to make a definite diagnosis and prescribe the most effective course of treatment.

Abdominal Pain↗
PubMed1989

The pathogenesis of graft-versus-host reaction in the intrahepatic bile duct. An immunohistochemical study.

Although intrahepatic bile duct injury following bone marrow transplantation is considered to be one feature of graft-versus-host disease, its developmental mechanism has not been clarified. In order to elucidate this aspect, an immunohistochemical study of the liver following human allogeneic bone marrow transplantation was made. Cytotoxic T lymphocytes (Tc) and natural killer cells (NK) were found in contact with intrahepatic bile duct epithelial cells showing degeneration and necrotic changes. These findings suggested a cytotoxic effect of these cells on bile duct epithelial cells. Abnormal expression of HLA class II (DR) antigen was recognized in intrahepatic bile duct epithelial cells following bone marrow transplantation. Cell injury was prominent in cells with weak DR antigen expression, whereas the cells demonstrating conspicuous expression appeared almost normal. There results suggest that abnormal expression of DR antigen plays an important role in the development of GVHD of the intrahepatic bile duct.

Bile Duct Diseases↗
PubMedDate not supplied

Etiologic significance of anatomic variations in the main intrahepatic bile ducts in hepatolithiasis.

Abnormal union of intrahepatic bile ducts has been suggested as a possible etiologic factor in the occurrence of intrahepatic stones. A series of 241 patients were examined by direct cholangiography, and anatomic variations in the intrahepatic bile ducts were classified into four types: Type A-1, normal union having a true right hepatic duct; Type A-2, absence of a right hepatic duct, with a trifurcation; Type B, posterior segmental duct draining into left hepatic duct; Type C, anterior segmental duct draining into left hepatic duct. The most dominant type was Type A-1, which occurred in 58.3 to 66.0 per cent of the cases, followed by Type A-2 with 12.5 to 19.8 per cent. Type B showed the lowest incidence, occurring in 4.5 to 10.4 per cent. No statistical difference existed in the distribution of the type of union of intrahepatic bile ducts on the one hand and the presence or absence of intrahepatic stones on the other. Thus, anatomic variations in the main intrahepatic bile ducts do not seem to be associated with hepatolithiasis, and their etiologic significance seems to be unlikely.

Adult↗
PubMed1994

Expression of tenascin, type IV collagen and laminin during human intrahepatic bile duct development and in intrahepatic cholangiocarcinoma.

Expression of tenascin, type IV collagen and laminin during human intrahepatic bile duct development and in cholangiocarcinoma was examined by immunohistochemistry. In the developing hilar bile ducts, tenascin was expressed in the mesenchyme around the epithelial cells migrating from the ductal plate into the mesenchyme at 10-14 weeks of gestation. Tenascin was also expressed in the mesenchyme around newly formed hilar bile ducts at 15-20 weeks of gestation, but its expression disappeared after 21 weeks of gestation. Type IV collagen and laminin were expressed around the ductal plate, around epithelial cells migrating from the ductal plate into the mesenchyme, and around newly formed hilar bile ducts, and their expression was present throughout fetal life. By contrast, in the development of peripheral bile ducts, tenascin expression was not found. Type IV collagen and laminin were identified around the ductal plate, migrating epithelial cells and peripheral bile ducts. In cholangiocarcinoma, tenascin and type IV collagen were expressed in the stroma, but laminin was not identified. These findings suggest that tenascin may play a role in hilar bile duct development and that type IV collagen and laminin may play a role in both hilar and peripheral bile duct development. Expression of tenascin and type IV collagen in the stroma of cholangiocarcinoma may be the result of malignant transformation of intrahepatic biliary epithelium; tenascin in peritumoral stroma may stimulate carcinoma cell proliferation and growth in cholangiocarcinoma.

Adult↗
PubMed2006

Endoscopic management of liver abscesses and cysts that communicate with intrahepatic bile ducts.

BACKGROUND AND STUDY AIMS: The formation of a communication between liver abscesses or cysts and intrahepatic bile ducts is an uncommon cause of significant bile leak. Surgical management of biliary fistulas is associated with high morbidity and mortality. We performed a prospective study of endoscopic management of this type of biliary fistula. PATIENTS AND METHODS: We studied 26 patients who had either liver abscesses or hepatic cysts that had ruptured into the intrahepatic bile ducts. The presence of a biliary fistula was suspected by jaundice and/or by the appearance of bile in percutaneous drainage effluent from a liver abscess and was confirmed by endoscopic retrograde cholangiopancreatography. Once the route of the fistula between the liver abscess or cyst and the intrahepatic bile duct had been defined by cholangiography, patients underwent treatment by sphincterotomy, and either biliary stenting or nasobiliary drainage. Nasobiliary drains or biliary stents (both 7 Fr) were placed according to standard techniques. Nasobiliary drains were removed when bile leakage stopped and closure of the fistula was confirmed by cholangiography; stents were removed after an interval of 4-6 weeks. RESULTS: Of a total of 525 patients with hepatic abscesses or cysts who were seen over a 5-year period, there were 26 patients who developed a demonstrable communication between liver abscesses (n = 20; 16 amebic, four pyogenic) or hydatid cysts (n = 6) and intrahepatic bile ducts (right intrahepatic bile ducts in 22 patients, left intrahepatic bile ducts in four patients). We performed either sphincterotomy with insertion of a nasobiliary drain (n = 20) or sphincterotomy with biliary stenting (n = 6). The fistulas healed in all patients after a mean time of 4 days (range 2-20 days) after endoscopic treatment. We were able to remove the nasobiliary drainage catheters and stents 6-34 days after their placement. CONCLUSIONS: In this case series, endoscopic therapy appears to be an effective mode of treatment for biliary fistulas complicating liver abscesses and cysts.

Adult↗