SEARCH · PubMed Health
Results for “Cholagogues and Choleretics”
Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
[Controlled double-blind clinical study of cinnametic acid, a new choleretic agent in hepatobiliary diseases].
Explore the source record for details and available documents.
Effect of gastrin I and gastrin II on canine bile flow.
The role of gastrin in the hormonal control of canine hepatic bile flow was evaluated. Because of the importance of the presence of sulfation of the carboxyl terminal peptide in the function of other cholecystokinetic hormones and peptides in the biliary tract, the choleretic properties of sulfated gastrin II were compared to the choleretic properties of nonsulfated gastrin I. Exogenous administration of gastrin I and II to dogs with chronic bile fistulas demonstrated that gastrin II, but not I, significantly increased hepatic bile flow. Chemical stimulation of the release of endogenous gastrin in dogs with denervated antral pouches did not increase hepatic bile flow, whereas a choleresis resulted when the innervated antrum was stimulated. Serum gastrin values obtained during the infusion of gastrin II at doses that produced a choleresis resulted in serum gastrin values that were greater than those produced by a more physiological stimulus, such as chemical antral stimulation. The results of this study suggest that only the sulfated gastrin II, not gastrin I, is a choleretic agent in dogs and only at pharmacological, not physiological doses.
[Synthetic choleretics: mechanism of action and secondary biochemical activity].
Explore the source record for details and available documents.
Effect of choleretics on biliary and urinary excretion of cholecystographic agents.
Two choleretic agents, taurocholate and cinchophen, were studied in the dog to determine their effect on both the biliary and urinary excretion of two related cholecystographic agents, iopanoic acid and iophenoxic acid. Liver concentrations were determined on biopsies. Trace amounts of radioactively labeled compounds were used for measurements. The effect of the choleretic agent was specific for the cholecystographic compound. Taurocholate increased both biliary and urinary excretion of iopanoic acid and decreased its intrahepatic level, but had no effect on iophenoxic acid. Cinchophen had no effect on iopanoic acid but increased both biliary and urinary excretion of iophenoxic acid. When examined against a pre-existing high rate of bile flow, the active choleretic increased, rather than decreased, the biliary concentration of the cholecystographic compound. The increased excretion in both bile and urine cannot be attributed simply to the lessened concentration gradient from plasma to bile, as proposed by others. The data are consistent with a direct action of the choleretic agent on hepatic mechanisms, either to decrease intracellular binding or to alter the characteristics of transport.
[Importance of Debray's test with a choleretic and morphine with concurrent assessment of enzymes in the diagnosis of hypertonic dyskinesia of the sphincter of Oddi (author's transl)].
Explore the source record for details and available documents.
The effects of synthetic prostaglandin analogs on canine hepatic bile flow.
The synthetic prostaglandin analogs 16, 16-dimethyl PGF2 alpha and 16, 16-dimethyl PGE2 were administered to dogs with chronic biliary and gastric fistulas. The effects of 16, 16 diMePGF2 alpha and 16, 16 diMePGE2 were evaluated on bile flow and composition and bile adenosine 3', 5' monophosphate (cyclic AMP) secretion. 16, 16 diMePGF2 alpha in doses of 0.125 and 0.25 microgram-kg-min significantly increased hepatic bile flow. The choleresis was characterized by increased chloride and bicarbonate secretion. Measurement by radioimmunoassay of bile cyclic AMP concentration demonstrated no evident increase in bile cyclic AMP secretion associated with the choleresis produced by 16, 16 diMePGF2 alpha. The administration of 16, 16 diMePGE2 in a dose range 0.01 to 1.0 microgram-kg-min did not significantly alter bile flow rates or composition. Bile erythritol-14C clearance, a measure of canalicular bile flow, was significantly increased by PGF2 alpha but not by 16, 16-dimethyl PGF2 alpha, suggesting that the mechanism of action of PGF2 alpha in stimulating hepatic bile flow may be different from that involved in 16, 16-dimethyl PGF2 alpha choleresis. The results of this study indicate that the synthetic PGF2 alpha analog produces a choleretic response not mediated by adenylate cyclase and associated with increased chloride and bicarbonate secretion.
[Piprozoline in clinical trials (author's transl)].
The tolerance and efficacy of ethyl (Z)-(3-ethyl-4-oxo-5-piperidino-thiazolidin-2-ylidene) acetate (piprozoline, Gö 919, Problin) were investigated in open and controlled clinical trials involving a total of 1545 patients and 1807 courses of therapy. The objective of this paper is to compare the experimental findings, some of which have already been published, with the results of the extensive clinical investigations. Despite the well-known problems associated with obtaining precise data on upper abdominal disorders, the evaluation of the available comprehensive clinical data has shown that probiline possesses definite therapeutic benefits confirming the experimental findings. Individual complaints such as bloating, upper abdominal pressure, meteorism and flatulence, nausea and vomiting, constipation, anorexia, and fat intolerance improved significantly under probiline therapy. Taking all the criteria into consideration, the overall results of the studies with probiline versus placebo in patients with gall-bladder diseases and intestinal disorders have proved that this choleretic substance is of therapeutic benefit. Serum bilirubin and alkaline phosphatase showed a significantly greater tendency to return to normal levels under probiline therapy than with placebo. The majority of conditions treated were of biliary origin. Aside from establishing the drug's therapeutic profile, the data published also show that the rate of side-effects was insignificant.
Choleretic and cholestatic effects of infused bile salts in the rat.
In rats, at low infusion rates taurocholate (TC), taurochenodeoxycholate (TCDC) and taurodeoxycholate (TCD) each produced an increase in bile flow of 20-50%. However, at high infusion rates (5-20 mumoles min-1kg-1) the cholestatic effects of the bile salts were revealed and the relative toxicity of the bile salts was seen to be TDC greater than TCDC greater than TC.
Cyclic AMP in secretin choleresis. Evidence for a regulatory role in man and baboons but not in dogs.
Cyclic AMP output in the bile in response to intravenous secretin was measured in 11 patients, 12 baboons, and 15 dogs. Secretin was given to patients with bile drainage tubes as an intravenous bolus (1 U per kg). In baboons and dogs both secretin infusion (4 U per kg per hr) and bolus injection (1 U per kg) were used. In baboons cyclic AMP was also determined in liver, extrahepatic duct tissue, and in perfusate from isolated segments of extrahepatic bile ducts. Secretin induced a marked choleresis in all three species. In humans, biliary cyclic AMP concentration increased an average (+/- 1 SE) of 68% +/- 12% and in baboons 4-fold, but no increase occurred in dogs. In baboons, cyclic AMP concentration increased in both bile duct tissue and perfusate from isolated bile ducts concomitant with secretin choleresis, but not in liver. In humans the choleretic effects of sodium dehydrocholate, aminophylline, and glucagon were compared to dibutyryl cyclic AMP (DBcyclic AMP). All agents increased bile flow 2- to 3-fold. Cyclic AMP concentration in bile markedly increased after glucagon and DBcyclic AMP but not after sodium dehydrocholate and aminophylline. We conclude that cyclic AMP is implicated in secretin choleresis in both humans and baboons, but not in dogs. The bile duct appears to be the site of cyclic AMP elaboration induced by secretin in baboons and probably is also in man.
[Clinical studies on the choleretic agent Febuprol (author's transl)].
In previous pharmacological experiments with the choleretic agent Febuprol, healthy subjects showed a significant increase in bile flow and its constituents in the acute experiment. As a consequence of these results we have carried out a double-blind cross-over therapeutic trial with Febuprol in 50 patients with a cholecystopathic symptom complex. After a 14 days' treatment (3 capsules daily) a significant improvement of the typical symptoms (feeling of fullness, pressure in the upper abdomen, meteorism, constipation, flatulence and nausea after food) was recorded in these patients. Moreover a significant lowering of the serum cholesterol level was noteworthy.
[Therapeutic effect of a pharmacologic combination of choleretics and digestive enzymes in exocrine pancreatic insufficiency].
Phosphorylcholine and homocysteine have an important choleretic action and also potentiate exocrine pancreatic secretion by way of stimulation and a more effective preparation of the substrate against attack by lipolytic enzymes. The protection offered by pancreatic enzymes in the correction of the digestive insufficiency in the endoluminal stage is also known. An analysis was therefore made of the action of an association of phosphorylcholine homocysteine and digestive enzymes in cases of exocrine pancreatic insufficiency and primary or secondary malabsorption. This action was evaluated on the basis of the reduction of elimination of steatorrhoea. For this purpose, faecal lipids were determined with the method proposed by van de Kramer et al. The most significant results were obtained in cases where digestive insufficiency was most marked, where correction of the pancreatic enzyme deficiency and improved biliary function were particularly required.
Absorption, distribution and excretion of a dihydroxydibutyl ether labelled with 14C in animals.
Kinetic studies were performed in rats, dogs and monkeys after oral administration of 14C-labelled dihydroxy-dibutyl ether (DHBE; Discinil), a known choleretic agent. The data presented indicate that the compound was intirely and readily absorbed and that it was excreted mainly with the urine in all the three species. The complete distribution pattern was investigated in rats. In most tissues high levels of radioactivity were already present after 10 min and the peak concentration was reached within the first 30 min. The decay was rapid and at the fourth hour only traces of radioactivity could be still detected in the tissues. Liver and kidney were the target organs for the radioactive material (which is in accordance with the activity and the excretory route of DHBE). The blood levels paralleled the general tissue distribution. The excretion of radioactivity was completed within 24 h in the three animal species and it took place by the urinary route, mainly witin the first 7--8 h.
Disposition of valproic acid in the rat: dose-dependent metabolism, distribution, enterohepatic recirculation and choleretic effect.
A specific gas chromatographic assay has been developed for measurement of valproic acid (VPA) and its major conjugated metabolites. In rats given single intravenous doses, the decline in blood concentration of VPA was dose-dependent and followed first-order kinetics only at the lowest dose. The time required for the maximum concentration of VPA, after completion of the brief distribution phase, to decline by 50% was 11.7, 41 and 125 min at doses of 15, 150 and 600 mg of NaVPA per kg, respectively. A secondary increase in drug concentration, abolished by exteriorization of the bile, was observed in all intact rats with all doses. Some 45 to 55% of the dose appeared in the bile in 5 hr as VPA glucuronide. Urinary excretion of VPA glucuronide in intact animals accounted for 23 and 51% of the 15 and 150 mg/kg doses, respectively. Tissue distribution studies in rats sacrificed 20 and 90 min after dosage with [14C] NaVPA (150 mg/kg) showed that the drug concentration was highest in blood, moderate in liver, kidney, heart and lung and low in brain, fat, testis and skeletal muscle. During this interval the drug concentration declined in all tissues, whereas the total conjugated metabolites in the small intestine increased from 7 to 28% of the administered dose. The large intestine contained 30 times as much free drug as conjugate. Reabsorption of free VPA, released by hydrolysis of conjugate in the large bowel, accounted for the secondary rise in concentration of VPA observed in blood after single doses. The major urinary metabolites, VPA-glucuronide and 2-n-propylgutaric acid, were identified by gas chromatography/chemical ionization mass spectrometry. Sodium VPA caused a dose-dependent stimulation of bile flow, the magnitude and duration of which closely followed the blood concentration of VPA.
Choleresis and cholestasis produced by infusion of taurocholic acid or taurodehydrocholic acid combined with BSP in the rhesus monkey.
To study the determinants of BSP Tm in rhesus monkeys, animals with indwelling silastic catheters were infused with sufficient BSP to produce a rising plasma concentration and normal saline or taurocholic acid 3.5 mumol/min, 7.0 mumol/min, or 10.5 mumol/min. BSP Tm was 3.84 +/- 0.11 mg/kg/10 min during normal saline infusion, 5.52 +/- 0.53 mg/kg/10 min during taurocholic acid 3.5 mumol/min, despite greater bile flow with the latter compound. Higher infusion rates of taurocholic acid inhibited BSP Tm and the proportion of conjugated BSP secreted into bile, as well as bile flow and bile acid secretion. Taurodehydrocholic acid 7.0 mumol/min produced similar but less marked effects. These results indicate that bile flow does not explain the effects of bile acids on BSP Tm and suggests that bile acids exert varying effects on BSP transport or binding in micelles. The cholestasis observed with combined BSP and higher bile acid infusion rates is probably due to inhibition of liver cell intermediary metabolism or to liver cell toxicity.
The biliary excretion of bucolome in the rat: a possible cause for choleresis.
Explore the source record for details and available documents.
The effect of rifampicin on liver blood flow, microsomal enzyme activity and bile flow in the rat.
Explore the source record for details and available documents.
Secretin-, glucagon-, and insulin-induced effects on bile flow and metabolism of isolated perfused canine and porcine liver.
Explore the source record for details and available documents.