Retrograde Intrabiliary Injection Research Articles

Three methods for measuring the increase in the capacity of the distended biliary tree in the rat produced by α-naphthylisothiocyanate treatment

The capacity of the distended biliary tree was measured in each rat by three techniques referred to as retrograde-intrabiliary-injection (RII), segmented-retrograde-intrabiliary-injection (SRII), and retrograde-pushback (RPB). Control rats, receiving by gavage 0.2 ml of olive oil daily for 8 consecutive days, were found 15 days after treatment to have distended capacities of 33.4 ± 2.7, 34.1 ± 3.4, and 31.6 ± 2.9 μl (mean ± SE) as obtained by the RII, SRII, and RPB techniques, respectively. In another group of rats, treated for 8 consecutive days with α-naphthylisothiocyanate (ANIT) (45 mg/kg, po) in 0.2 ml of olive oil, the RII, SRII, and RPB techniques estimated distended biliary capacity 15 days after the last treatment to be 48.0 ± 1.6, 47.5 ± 1.4, and 46.8 ± 1.3 μl, respectively. In control animals the two-way analysis of variance showed no significant difference occurred between the three methods. For each of the three methods, the mean distended biliary tree capacity of the ANIT-treated rats was significantly greater than the control rats, p < 0.02. No significant difference was found between control and ANIT-treated rats for mean liver weights and bile flow rates. Thus, the increase in distended biliary capacity with ANIT treatment was not accompanied by any change in liver weight or bile flow rate.

Influence of retrograde volume and short time cholestasis on the biliary reabsorption of sulfobromophthalein sodium (BSP) and phenol 3,6 dibromphthalein disulfonate (DBSP) from the rat biliary tree after retrograde intrabiliary injection (RII).

The retrograde intrabiliary injection (RII) technique was used to study the reabsorption of equimolar doses (1,2 mumol) of sulfobromophthalein sodium (BSP) and its analogue phenol 3,6 dibromphthalein disulfonate (DBSP) from the rat biliary tree under the experimental conditions established in this study i.e. variation of retrograde volumes injected and of short time cholestasis. RII was performed with a microliter syringe joined to a cannula positioned in the proximal third of the common bile duct. This technique guaranteed accurate administration of microliter quantities, also free bile flow could be reinitiated 3 - 5 sec after RII. Bile samples were collected in 2, 5 min intervals up to the 5th min, then in 5 min intervals up to the 15th min, and the following 15 min up to the 30th min and analysed for compounds administered by RII. No significant differences in the biliary reabsorption of BSP and DBSP after RII could be detected. Increasing retrograde volumes of 20, 40, 60, 110, and 160 mul lead to decreasing percent recoveries in the bile in the first 2,5 min after RII (88,0 +/- 3,8 - 15,6 +/- 3,1) when bile flow was started at once after RII. An inverse correlation between retrograde volume and percent recoveries was found. Increasing duration of cholestasis (bile flow was started at once, 0,5 min, 3 min, 6 min, and 30 min after RII) results in decreasing percent recoveries of BSP and DBSP in the first 2,5 min after free bile flow was reinitiated (52,7 +/- 3,6 - 20,0 +/- 1,2). A time dependent proportional effect could be detected. Furthermore in the case of BSP concomitant with increasing cholestasis increasing amounts of BSP - conjugates were found in the bile supporting the idea of a continuing ductular - hepatocellular circulation even during complete obstruction of the common bile duct.

Influence of dehydrocholate sodium on the biliary reabsorption of sulfobromophtalein sodium from the rat biliary tree after retrograde intrabilary injection.

Bilary re-excretion of sulfobromophthalein sodium (BSP) (1.2 mumol/rat) after retrograde intrabilary injection is markedly inhibited by dehydrocholate sodium (Decholin) given intravenously as a constant infusion (3.1 mumol/min/kg body weight) or as a bolus injection (24.8 mumol/rat) to rats. Most interestingly Decholin demonstrates the same inhibitory effects on the biliary re-excretion of BSP when it is administered by retrograde intrabiliary injection (24.8 mumol/rat) together with the dye. In contrast to the inhibition of biliary re-excretion of BSP its biliary reabsorption from the biliary tract seems to be rather increased: about 80-85% of 1.2 mumol BSP are reabsorbed in all sets of experiments with Decholin in comparison to about 65% to the control group. Combined with histological data it is suggested that reabosorption of BSP after retrograde intrabiliary injection occurs at the ductular site whereas re-excretion takes place at the cannalicular membrane of the hepatocyte.

Increased “bile duct-pancreatic fluid” flow in rats pretreated with carbon tetrachloride

Retrograde intrabiliary injection experiments in CCl 4-pretreated (1 ml/kg, ip, 24 hr) rats suggested that the retrogradely injected solution was being diluted in the common bile duct portion of the biliary tree. This dilution was substantiated in subsequent experiments by a double-cannulation technique. To collect hepatic bile, a PE 10 cannula was placed in the proximal portion of the common bile duct near the liver hilus. To collect “bile duct-pancreatic fluid,” the distal portion of the ligated common bile duct was cannulated near the duodenum. CCl 4 pretreatment produced a 40% decrease in hepatic bile flow (57 ± 6 mg/min/kg, control, vs 35 ± 4, CCl 4, mean ± SE) and a 600% increase in bile duct-pancreatic fluid flow (1.6 ± 0.3 mg/min/kg, control, vs 9.5 ± 1.8, CCl 4). The enhanced bile duct-pancreatic fluid flow did not involve a change in the rate of protein and amylase excretion from the pancreas. Also CCl 4 produced a decrease in the secretory pressure of hepatic bile and an increase in that of bile duct-pancreatic fluid. Thus, CCl 4 has the interesting action of increasing bile duct-pancreatic fluid flow at the same time it is decreasing hepatic bile flow.

Increased “bile duct-pancreatic fluid” flow in chlorinated hydrocarbon-treated rats

The following chlorinated hydrocarbons, CCl 4, Cl 2CH 2, chloroform, 1,1,2-trichloroethane, 1,1-dichloroethylene, 1,1,2-trichloroethylene, and 1,1,2,2-tetrachloroethylene, were administered 1 day before testing. The test consisted of a retrograde intrabiliary injection of [ 3H]inulin followed by a 6-min period of occlusion, to hold the [ 3H]inulin solution in the biliary tree, and then collecting and analyzing each drop of bile. The content of [ 3H]inulin in the drops from the distal portion of the biliary tree was diluted by increased excretion of “bile duct-pancreatic fluid” into the duct system during the 6-min occlusion period. An increase in bile duct-pancreatic fluid flow in chlorinated hydrocarbon-treated rats was directly demonstrated by cannulating the common bile duct at the proximal bifurcation (to collect hepatic bile) and distally at the duodenum (to collect bile duct-pancreatic fluid). The results showed that the chlorinated hydrocarbons produced an increase in bile duct-pancreatic fluid flow. The increase in this distal fluid flow was not correlated to a rise in SGPT activity or extent of liver cell necrosis because both 1,1-dichloroethylene, which produced high SGPT activity and necrosis, and chloroform, low SGPT and no necrosis, increased bile duct-pancreatic fluid flow to a similar extent.

Differences of reabsorption of unconjugated BSP and BSP-glutathione from the rat biliary tree after retrograde intrabiliary injection.

It has been shown that water and electrolytes are reabsorbed from the biliary tract of the rat. Furthermore there are some suggestions for the reabsorption of organic compounds during their passage down the biliary tract. Our results presented in this paper demonstrate a different mode of biliary excretion of unconjugated BSP [BSP-U] and BSP- glutathione [BSP-GSH] after retrograde intrabiliary injection, BSP-GSH is excreted to a much greater extent than BSP-U within the first 5 minutes after retrograde administration. In other terms BSP-GSH is reabsorbed to a lesser extent than BSP-U. Additionally the reabsorption of BSP-U and BSP-G after retrograde injection seems to be dependent on the concentration and the contact time in the biliary tree. It is suggested that the different biliary excretion of BSP-U and BSP-GSH after intravenous injection might be explained partly by a different reabsorption mode.

Route of Flow and Micropathology Resulting from Retrograde Intrabiliary Injection of India Ink and Ferritin in Experimental Animals: A combined light- and electron-microscopic study

India ink and/or ferritin were used as tracers to follow the route taken by material injected retrograde into the biliary system of mice, rats, and rabbits. Tissue was prepared for light- and electron-microscopic study by routine techniques. Tracer material was fairly evenly distributed through the liver, filling many parts of the ductal system. India ink suspended in normal saline usually was found widely distributed in liver sinusoids. Electron microscopy showed that aggregates of platelets sometimes were associated with tracer material. Isolated small groups of hepatic cells contained dense deposits of India ink filling part or all of the cytoplasm. Marked cellular disruption was evident in electron micrographs of similar areas. It was concluded that retrograde intrabiliary injection of material disrupts hepatic cells to allow escape into sinusoids through the spaces of Disse. It is proposed that retrograde injection of such materials as radiocontrast media may cause similar micropathology and entry of biliary contents into the circulation.

Bile formation in guinea pigs: analysis with inert solutes of graded molecular radius.

ARTICLESBile formation in guinea pigs: analysis with inert solutes of graded molecular radiusEL ForkerEL ForkerPublished Online:01 Jul 1968https://doi.org/10.1152/ajplegacy.1968.215.1.56MoreSectionsPDF (2 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformationCited ByCholangiocyte anion exchange and biliary bicarbonate excretionWorld Journal of Gastroenterology, Vol. 12, No. 22Fetal excretion of the fluorescent bile acid derivative cholylglycylamido-fluorescein (FITC-GC) by the rat placenta-maternal liver tandemPlacenta, Vol. 19, No. 1Ursodeoxycholate-induced hypercholeresis in cirrhotic rats: Further evidence for cholehepatic shuntingHepatology, Vol. 20, No. 4Hepatic excretion and metabolism of polyethylene glycols and mannitol in the catJournal of Hepatology, Vol. 17, No. 1The pattern of vasopressin-induced reduction in biliary output of cholephilic probes in the rat can be mimicked by dialysisHepatology, Vol. 14, No. 1Adrenergic influence on bile secretion-an experimental study in the catActa Physiologica Scandinavica, Vol. 140, No. 2Biliary excretion of different sized polyethylene glycols in the catJournal of Hepatology, Vol. 11, No. 2Demonstration of vesicular-dependent bile flow in the sucrose-loaded ratGastroenterology, Vol. 99, No. 2The effects of hypertonic glucose solutions on hepatic bile formationJournal of Hepatology, Vol. 11, No. 1Cellular Mechanisms of Hepatic Fluid and Electrolyte Transport1 January 2011Effect of molecular charge on para- and transcellular access of horseradish peroxidase into rat bileHepatology, Vol. 9, No. 6The Passage of Molecules into Bile: Paracellular and Transcytotic PathwaysBiliary clearance of inert carbohydratesGastroenterology, Vol. 94, No. 1Mechanisms of Bile Secretion and Hepatic TransportPermeability characteristics of the guinea pig biliary apparatusHepatology, Vol. 6, No. 6Mechanisms of Bile Secretion and Hepatic TransportPostnatal development of hepatic bile formation in the rabbitDigestive Diseases and Sciences, Vol. 30, No. 6Relation between molecular weight and pulmonary absorption rate of lipid-insoluble compounds in neonatal and adult ratsBiochemical Pharmacology, Vol. 32, No. 17Cellular mechanisms of bile formationGastroenterology, Vol. 82, No. 2Effect of Ethanol on Formation of Bile1 February 2008 | Alcoholism: Clinical and Experimental Research, Vol. 5, No. 1Tissue Distribution and Metabolism of Drugs V: Effect of Secretin and Pancreozymin on Drug Transport in Rabbit PancreasJournal of Pharmaceutical Sciences, Vol. 69, No. 1Evaluation of hepatobiliary function in the rat by the segmented retrograde intrabiliary injection techniqueBiochemical Pharmacology, Vol. 29, No. 2Characteristics of inert solute clearance by the monkey liverGastroenterology, Vol. 76, No. 2Phalloidin-induced cholestasis in the rat: Relation to changes in microfilamentsGastroenterology, Vol. 75, No. 3Erythritol and mannitol clearances with taurocholate and secretin-induced cholereses.J L Barnhart, and B Combes1 February 1978 | American Journal of Physiology-Endocrinology and Metabolism, Vol. 234, No. 2Die LeberHepatic Bile FormationNew England Journal of Medicine, Vol. 295, No. 26Canalicular Bile Production in ManEuropean Journal of Clinical Investigation, Vol. 5, No. 1Principles of Biliary SecretionBiliäre Clearance und intrahepatische Verteilung von Sucrose und Natrium-Ferrocyanid bei Äthinylöstradiol-CholestaseEffect of osmotic pressure on spontaneous afferent discharge in the nerves of the perfused rabbit liverPfl�gers Archiv European Journal of Physiology, Vol. 361, No. 1Mechanisms and Control of Secretion of Bile Water and ElectrolytesGastroenterology, Vol. 66, No. 2Bile SecretionClinics in Gastroenterology, Vol. 2, No. 1The influence of secretin on the elimination of14C-Edrophonium in bileExperientia, Vol. 28, No. 11Excretion of 14C-edrophonium and its metabolites in bile: role of the liver cell and the peribiliary vascular plexus19 July 2012 | British Journal of Pharmacology, Vol. 44, No. 3Canalicular Bile flow and Bile Secretory PressureGastroenterology, Vol. 59, No. 6Rapid passage of mannitol into liver and bileLife Sciences, Vol. 9, No. 17Pathophysiology of cholestasisHuman Pathology, Vol. 1, No. 1 More from this issue > Volume 215Issue 1July 1968Pages 56-62 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1968.215.1.56PubMed5659343History Published online 1 July 1968 Published in print 1 July 1968 Metrics