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At least 523 records · Page 29Linked to original sources
PubMed1983

[Cefmetazole excretion into the bile after hepatic portojejunostomy in congenital bile duct atresia].

Antibiotics excretion into the bile was studied using CMZ which was administered by drip infusion in 12 postoperative cases of congenital bile duct atresia patients who had hepatic portojejunostomy with SURUGA II type enterostomy with the following results. Group I (correctable type children, with good bile flow, no jaundice): Excellent excretion was almost the same as that seen in adult patients. Group IIa (uncorrectable type children, with good bile flow, no jaundice): Excretion was poor but good depending on the amount of bile flow and liver function. Group IIb (uncorrectable type children, with poor bile flow, jaundice): Excretion was very poor. Group III (uncorrectable type infants, with good flow, no jaundice): Excretion was good depending on the amount of bile flow and liver function. Our study indicates that antibiotics excretion into the bile in children is closely related to the condition of the hepatic function and biliary passage.

Age Factors↗
PubMed1978

[Effect of progesterone and phenylbutazone on bile flow and bile acid excretion in male Wistar rats].

Bile flow and excretion of monohydroxy-, dihydroxy- and trihydroxy bile acids (MBA, DBA and TBA) were estimated after acute and subacute progesterone and phenylbutazone pretreatment in adult male Wistar rats in three one-hour periods. Different pretreatment with sunflower oil did not influence bile flow and excretion of DBA and TBA. MBA were not detected. Different administration of progesterone and phenylbutazone did not significantly change the TBA/DBA ratio. Progesterone administration (50 mg/kg b. w. i. p.) 2 hours before bile sampling increased bile flow and bile acid excretion in the third one-hour period. After 3 days of pretreatment with progesterone (3 X 50 mg/kg b. w. i. p.) bile flow and TBA-excretion were diminished. Phenylbutazone (100 mg/kg b. w. i. p.) increased bile flow and TBA-excretion both after acute and subacute administration.

Animals↗
PubMed1995

The protective effect of hydrophilic bile acids on bile acid hepatotoxicity in the rat.

Taurochenodeoxycholate (TCDC) (or taurocholate, TC) excessively i.v. infused in rats causes an acute cholestasis accompanied by an excessive excretion of various proteins (lactate dehydrogenase, LDH, albumin, etc.) into the bile. This cholestasis was initially found to be effectively prevented by a simultaneous infusion of tauroursodeoxycholate (TUDC). Later this property was found to be shared by glycoursodeoxycholate (GUDC) and tauro (and glyco) alpha and beta-muricholate (MC) all known to be relatively hydrophilic. The extent of the preventative effect appears to be comparable for taurine and glycine conjugates of all three bile salts (UDC, alpha-MC and beta-MC). An albumin leakage into the bile enhanced by TCDC infusion appears to be mainly from albumin in the serum, since i.v. injected 125I-human serum albumin excretion into the bile paralled the rat albumin excretion. Despite very drastic biochemical abnormalities induced by TCDC infusion, morphological correlates in the liver are scarce both from light and electron microscopic examinations, the only correlate with biochemical parameters being a sporadic necrosis of hepatocytes, especially in the periportal areas. Although there is not sufficient morphological evidence, it appears that TCDC infusion causes a direct communication between serum and bile leading to a rapid leakage of large molecules such as albumin and even gamma-globulin. Conjugates of hydrophilic bile salts such as UDC, alpha-MC and beta-MC efficiently prevent such bile abnormalities but their hydrophilicity is not the sole determinant of this property since a more hydrophilic bile salt such as taurodehydrocholate does not possess this property. The underlying mechanism(s) for this protective property remains uncertain.

Albumins↗
PubMed1996

Postoperative bile peritonitis caused by division of an aberrant bile duct in the left triangular ligament of the liver.

A 61-yr-old man underwent Billroth I gastrectomy for an advanced cancer in the corpus of the stomach. On the first postoperative day, fresh bile discharged from the penrose drains, which had been placed in Winslow's foramen, and the volume of bile discharge subsequently increased. Leakage from the gastroduodenal anastomosis was excluded by gastroduodenography. Exploratory relaparotomy showed bile peritonitis with much more bile retention in the left subphrenic space. The origin of bile leakage could not be traced despite close examination of all the extrahepatic biliary tract and the liver surface. Intraoperative cholangiography through the cystic duct after cholecystectomy revealed that the bile leakage originated from an aberrant bile duct present in the free edge of the left triangular ligament (appendix fibrosa hepatis), which had been unintentionally cut at the primary operation. Knowledge of this anatomical structure is important and proper ligation is recommended when dissecting the appendix fibrosa hepatis to avoid postoperative bile peritonitis and the need for a relaparotomy.

Bile↗
PubMed1977

[Effect of chenic acid on bile lipid composition and on metabolism of bile acids in lithiasis patients].

Gallbladder bile unsaturated with cholesterol is a prerequisite for gallstone dissolution. Chenodeoxycholic (chenic) acid ingestion by patients with gallstones induces saturated bile to become unsaturated. Additionally, chenic acid becomes the predominant bile acid in bile and the chenic acid and total bile acid pools increase in a majority of such patients. Most importantly, the hourly secretion of cholesterol decreases during chenic therapy such that the cholesterol to bile acid ratio in bile is significantly lower and bile becomes unsaturated with cholesterol. Preliminary evidence suggests that the mechanism of action of chenic acid may relate to a suppression of the rate limiting hepatic enzyme for cholesterol synthesis, HMGCoA reductase.

Bile↗
PubMed1998

[The bile acid and bile lipid spectrum of the migrant population of the Asian North with biliary tract diseases].

AIM: The study of biochemical bile composition in Asian North migrants with biliary diseases (BD). MATERIALS AND METHODS: The diagnosis of BD was made upon clinical examination, ultrasound scanning, duodenal intubation in 329 examinees. The bile was examined for total bile acids, total cholesterol, total phospholipids and bile acid spectrum. RESULTS: Cholelithiasis patients were found to have high index of bile cholesterol saturation, high level of deoxycholic acid and low ratio primary/secondary bile acids. CONCLUSION: Changes in bile lipid spectrum are the leading cause of forming bile concrements in migrant population of the high altitudes.

Adult↗
PubMed1997

Imaging supramolecular aggregates in bile models and human bile.

Investigation of cholesterol crystallization is essential for the understanding of gallstone formation. Previous work has revealed a variety of aggregates of different sizes and shapes prior to the appearance of "classical" plate-like cholesterol monohydrate crystals both in native biles and model systems. In this article, we review existing data based on various microscopic techniques and present data on microstructural pathways leading to cholesterol crystal formation in two different bile models and in native bile. In continuation of our recent investigation of microstructures in nucleating human bile, we now present data suggesting that polymorphism is not limited to complex native bile, but also appears in two, simplified model systems. These studies employed cryo-transmission electron microscopy (cryo-TEM) and video-enhanced light microscopy, using Nomarski optics (VELM). Only the combined use of these two complementary, non-perturbing direct methods can cover the whole range of microstructures ranging from a few nanometers to several microns. Concentrated isotropic solutions of bile models, composed of cholesterol, lecithin and taurocholate, were diluted to induce cholesterol supersaturation and start an evolution of microstructures, leading to cholesterol crystallization. Initially, small spheroidal micelles were observed by cryo-TEM. Subsequently, uni-, oligo- and multilamellar vesicles, compatible with structures seen at the same time by VELM, appeared in coexistence with micelles. Thereafter, during a dynamic phase of cholesterol crystallization, filaments, tubular and helical microstructures, as well as classical plate-like cholesterol monohydrate crystals were noted by light microscopy. Eventually, large plate-like crystals were observed by VELM, while cryo-TEM revealed only small spheroidal micelles. The crystallization process in native human bile during ex vivo incubation was found to bear close resemblance to the findings in the model systems, further supporting the applicability of these systems to the exploration of microstructural aspects of nucleating human bile.

Bile↗
PubMed1996

Stimulation of bile acid independent bile flow with bromo-cyclic guanosine monophosphate.

The second messenger, cyclic guanosine monophosphate (cGMP), mediates the actions of nitric oxide, natriuretic peptides, and microbial toxins on cellular contractility and electrolyte movement. Because both hepatocellular contractility and electrolyte secretion participate in bile formation, we investigated the actions of cGMP on this process in intact liver. In rat liver perfused with 8-bromo-cyclic GMP (bcGMP) at 0.5 and 3 micromol/min, bile flow increased by 5% and 31%, respectively. The biliary excretion of the bile acid, taurocholate ([3H]-labeled; 1 micromol/min) and of the organic anion, bromosulfophthalein ([35S]-labeled; tracer dose), was unchanged. The paracellular and transcytotic pathways of biliary excretion, assessed by horseradish peroxidase (HRP), were unaffected. BcGMP was concentratively secreted into bile and the accompanying 30% increase in the biliary clearance of erythritol suggested that the choleresis was primarily osmotic in nature. Unlike cyclic adenosine monophosphate (cAMP), which stimulates bile acid dependent bile flow and transcytosis, bcGMP increased bile acid independent bile flow mainly as a result of its concentrative biliary secretion.

Animals↗
PubMed1982

Bile acid malabsorption and bile acid diarrhea in intestinal resection.

Bile acid fecal excretion and dihydroxy bile acid concentration in the fecal water of patients with large (N = 6) and small (N = 8) ileal resection, colectomy (N = 5), and healthy controls (N = 10) have been studied in order to evaluate the degree of bile acid malabsorption and the occurrence of bile acid diarrhea in intestinal resections of different extent. Bile acid malabsorption was severe in large ileal resections, mild in small ones, and slight in colectomy. The fecal pH seems to be a limiting factor in the occurrence of a bile acid diarrhea, playing a critical role in determining the dihydroxy bile acid solubility in the fecal water. These results seem to suggest that the bile acids may induce water secretion in the colon not only in small but also in large ileal resections.

Adult↗
PubMed1989

Experimental detachment of the canine bile duct to evaluate mechanisms of the dilated bile duct.

The factors inducing biliary dilatation were studied morphologically and functionally by cholangiography and cholangiomanometry in experimental models of chronic biliary dilatation. These models were produced by four methods: Constriction of the lower bile duct (Group 1), formalin infusion into the duodenal papilla (Group 2), detachment of the extrahepatic bile duct (Group 3), and sphincterotomy (Group 4). Biliary dilatation was observed in the first three groups but not in the fourth group. An increase in the intraductal pressure due to blockage of the biliary outflow tract was considered to be the cause of biliary dilatation in Group 1 and 2. In Group 3, the function of the lower bile duct, including the papilla was intact, and reduced resistance of the bile duct wall and due to the loss of the support from the surrounding connective tissue was considered to have induced biliary dilatation. These results suggest that experimental chronic biliary dilatation can be produced by two approaches: 1) Blockage of bile flow in the papilla or the bile duct, and 2) detachment of the bile duct without disturbing bile flow.

Animals↗
PubMed2000

Protective effect of the bile salt hydrolase-active Lactobacillus reuteri against bile salt cytotoxicity.

Bacterial bile salt hydrolysis is considered a risk factor for the development of colon cancer because of the risk of forming harmful secondary bile salts after an initial deconjugation step. In this study, the influence of enhanced bacterial bile salt transformation by the bile salt hydrolase-active Lactobacillus reuteri was studied in batch culture using the microbial suspension of the Simulator of the Human Intestinal Microbial Ecosystem; (SHIME), which was supplemented with oxgall at 5 g/l or 30 g/l. Changes in the fermentative capacity of the microbial ecosystem and the (geno)toxic properties of the SHIME supernatants were investigated. Increasing concentrations of oxgall inhibited the fermentation. Transient cell toxicity was observed for samples supplemented with 5 g oxgall/l, while samples with 30 g oxgall/l exhibited toxicity. The results of the haemolysis test suggest that the detrimental effects were probably due to the membrane-damaging effects of bile salts. In all cases, the adverse effects could be counteracted by the addition of 7.5 +/- 0.5 log10 CFU L. reuteri/ml. Plausible mechanisms for the protective properties of L. reuteri could involve a precipitation of the deconjugated bile salts and a physical binding of bile salts by the bacterium, thereby making the harmful bile salts less bioavailable.

Amidohydrolases↗
PubMed1979

Partitioning of bile acids into subcellular organelles and the in vivo distribution of bile acids in rat liver.

1. The subcellular distribution of conjugates of cholic acid and chenodeoxycholic acid between cytosol, nuclei, mitochondria and microsomes in rat liver has been determined. 2. The partition coefficients for the distribution of these bile acids between subcellular fractions and buffer have been measured and used to construct a compartmental model of the amounts of conjugated bile acids present in the different subcellular organelles in vivo. 3. This model indicates that a large percentage of the bile acid in the rat liver is found in the nuclear fraction; 42% of the cholic acid conjugates and 27% of the chenodeoxycholic acid conjugates. Substantial amounts of bile acid are also present in microsomes and mitochondria suggesting that published estimates of the amounts of bile acids in these fractions are underestimates. 4. The model also allows the amount of bile acid which is in free solution in cytosol to be determined; 10.9% of the cholic acid conjugates and 4.1% of the chenodeoxycholic acid conjugates in rat liver were present in this fraction. Knowlege of the amount of free bile acid allows possible roles of the cytosolic bile binding proteins to be assessed.

Animals↗
PubMed1990

Oxidation and reduction of bile acid precursors by rat hepatic 3 alpha-hydroxysteroid dehydrogenase and inhibition by bile acids and indomethacin.

Enzyme kinetics of purified rat hepatic 3 alpha-hydroxysteroid dehydrogenase for bile acid precursors and effects of bile acids and indomethacin on those activities were studied. This enzyme catalyzed the oxidoreduction of the C3 position of bile acid precursors. Km for 7 alpha, 12 alpha-dihydroxy-5 beta-cholestan-3-one (1.6 microM) was markedly lower than Km for 7 alpha-hydroxy-5 beta-cholestan-3-one (28 microM) but Vmax was similar. Km for 3 alpha, 7 alpha-dihydroxy-5 beta-cholestane (12 microM) was lower than Km for 3 alpha, 7 alpha, 12 alpha-trihydroxy-5 beta-cholestane (150 microM) although Vmax/Km values were similar for both compounds. Bile acids and indomethacin inhibited the reduction of 3-oxo bile acid precursors. NADPH inhibited the binding of lithocholic acid (3 alpha-hydroxy-5 beta-cholanic acid) by 3 alpha-hydroxysteroid dehydrogenase. These data suggest that intrahepatic bile acid concentrations may affect the reduction of 3-oxo-bile acid precursors and intrahepatic redox conditions may affect intracellular bile acid transfer.

3-Hydroxysteroid Dehydrogenases↗
PubMed1993

Bile salt-stimulated lipase in human milk. Evidence that bile salt induces lipid binding and activation via binding to different sites.

Human milk bile salt-stimulated lipase ensures efficient triacylglycerol utilization in breast-fed newborns. For activity against long-chain triacylglycerol, primary bile salts are a prerequisite. Bile salts also protect the enzyme from inactivation by intestinal proteases. We have studied the effect of different bile salts on activation, protease protection, lipid binding, and enzyme inactivation, caused by an arginine modifying agent. Based on the results we propose a model involving two bile salt binding sites; one activation-site specific for primary bile salt, and another, less specific, lipid binding promoting site at which also secondary bile salt binds. Binding to this latter site induces binding of enzyme to emulsified substrates but binding promoting site at which also secondary bile salt binds. Binding to this latter site induces binding of enzyme to emulsified substrates but without subsequent lipolysis.

Bile Acids and Salts↗
PubMed1977

Sterol and bile acid metabolism during development. 1. Studies on the gallbladder and intestinal bile acids of newborn and fetal rabbit.

Bile acid composition and content in the intestine and gallbladder of newborn and fetal rabbits were investigated. Unlike the circumstances in adult rabbits, the bile acids were conjugated with both taurine and glycine. The major bile acids of the fetus and newborn rabbit were cholic acid, chenodeoxycholic acid, and deoxycholic acid. This is different from the known bile acid composition of adult rabbits, in which deoxycholic acid is the major bile acid (greater than 80%). The proportion of chenodeoxycholic acid was higher in the fetal than in the newborn tissues. The total bile acid pool in the newborn was higher than in the fetus. In the fetus, large proportions of bile acids (60.9%) were associated with the gallbladder fraction, whereas in the newborn the bulk of the bile acids were found with the intestinal fraction (64.4%).

Animals↗
PubMed1998

Expression of epithelial-cadherin, alpha-catenin and beta-catenin during human intrahepatic bile duct development: a possible role in bile duct morphogenesis.

BACKGROUND/AIMS: Cell adhesion molecules play an important role in the morphogenesis of developing organs. However, little is known about their expression during intrahepatic bile duct development. METHODS: We immunohistochemically investigated the expression of E-cadherin (E-Cad), alpha-catenin (A-Cat) and beta-catenin (B-Cat) during human intrahepatic bile duct development, using 31 fetal livers of various gestational ages. The developmental stages of bile ducts were classified into the ductal plate, migrating biliary cells (remodeling stage), and immature bile ducts (remodeled stage). RESULTS: E-Cad was broadly and strongly expressed in the ductal plate with a cytoplasmic pattern, heterogeneously and weakly expressed in the migrating biliary cells with a cytoplasmic pattern, and broadly and strongly expressed in immature bile ducts with a membranous pattern. A-Cat was broadly and strongly expressed in the ductal plate with a membrane pattern, broadly and moderately expressed in the migrating biliary cells with a membranous pattern, and broadly and strongly expressed in immature bile ducts with a membranous pattern. In contrast, expression of B-Cat was weak or slight in the ductal plate, but B-Cat was expressed broadly and strongly with a membranous pattern in migrating biliary cells and in immature bile ducts. Immature hepatocytes rarely expressed E-Cad and A-Cat, but expressed B-Cat with a membranous pattern throughout development. CONCLUSIONS: These results suggest that E-Cad, A-Cat and B-Cat are involved in the normal developmental morphogenesis of human intrahepatic bile ducts.

Bile Ducts, Intrahepatic↗
PubMed1989

Bile and stone analysis in two infants with brown pigment gallstones and infected bile.

Two infants under 3 mo of age who presented with obstructive jaundice secondary to cholelithiasis are reported. Neither infant had any congenital anatomic abnormality of the biliary tract leading to stasis, yet both had cultures of gallbladder bile that grew abundant bacteria. In both, recovery of gallbladder bile and sludge or actual stones allowed a detailed analysis of bile and stone composition. Bile was not saturated with cholesterol. In both cases, unconjugated bilirubin accounted for a large percentage of the total bile biliary pigments measured, and stercobilin was present in gallbladder bile. Bile beta-glucuronidase activity was higher when measured at the optimal pH of bacterial rather than tissue beta-glucuronidase. Analysis of stone morphology and composition showed characteristics of brown pigment gallstones with a layered appearance and the presence of calcium palmitate. This is the first report of detailed bile and stone analysis in infants and supports the hypothesis that brown pigment gallstones form spontaneously in infants who have bacterial infections in the biliary tract.

Bile↗
PubMed1997

Quantitative estimations of the contribution of different bile acid pathways to total bile acid synthesis in the rat.

BACKGROUND & AIMS: Cholesterol degradation to bile acids occurs via "classic" or "alternative" bile acid biosynthetic pathways. The aim of this study was to assess the contributions of these two pathways to total bile acid synthesis in vivo. METHODS: Rats with biliary fistulas were infused with squalestatin for 24 and 48 hours; specific activities of cholesterol 7 alpha-hydroxylase (C7 alpha H) and sterol 27-hydroxylase (S27H) and rates of bile acid synthesis were determined. RESULTS: Continuous squalestatin infusion (15 micrograms/h) decreased C7 alpha H specific activities to 4% and 12% of paired biliary fistula controls at 24 and 48 hours, respectively (P < 0.05) without any changes in S27H specific activities (82% and 95% of controls). At 24 hours, bile acid synthesis decreased to 43% (P < 0.05) but returned to 87% at 48 hours (P = NS). Cholic acid synthesis decreased at 24 hours but returned to control levels at 48 hours. Similar changes in C7 alpha H, S27H, and bile acid synthesis were observed in primary rat hepatocytes after addition of squalestatin (1.0 mumol/L). CONCLUSIONS: In the face of persistent suppression of C7 alpha H and the classic pathway, an alternative pathway becomes a main pathway of bile acid synthesis capable of generating cholic and chenodeoxycholic acids. The observed induction of bile acid synthesis via an alternative pathway or pathways represents an important mechanism for maintenance of cholesterol homeostasis in the rat.

Animals↗