Heavy water decreases bile salt-independent bile flow and increases paracellular permeability in the perfused rat liver

1989 ◽  
Vol 9 ◽  
pp. S41
Author(s):  
A. Hirlinger ◽  
H. Sägesser ◽  
J. Reichen
Keyword(s):  
Bile Salt ◽  
Rat Liver ◽  
Heavy Water ◽  
Bile Flow ◽  
Paracellular Permeability ◽  
Perfused Rat Liver

scholarly journals Acute effects of cholestatic and choleretic bile salts on vasopressin- and glucagon-induced hepato-biliary calcium fluxes in the perfused rat liver

1992 ◽  
Vol 283 (2) ◽  
pp. 575-581 ◽  
Author(s):  
Y Hamada ◽  
A Karjalainen ◽  
B A Setchell ◽  
J E Millard ◽  
F L Bygrave
Keyword(s):  
Bile Salt ◽  
Rat Liver ◽  
Strong Correlation ◽  
Bile Flow ◽  
Bile Salts ◽  
Perfused Rat Liver ◽  
Acute Effects ◽  
Calcium Fluxes ◽  
Principal Effect

The effects were investigated of the choleretic bile salt glycoursodeoxycholate (G-UDCA) and of the cholestatic bile salt taurochenodeoxycholate (T-CDCA) on changes in perfusate Ca2+, glucose and oxygen and in bile calcium and bile flow induced by the administration of (a) vasopressin, (b) glucagon and (c) glucagon plus vasopressin together to the perfused rat liver [Hamada, Karjalainen, Setchell, Millard & Bygrave (1992) Biochem. J. 281, 387-392]. G-UDCA itself increased the secretion of calcium in the bile several-fold, but its principal effect was to augment each of the above-mentioned metabolic events except glucose and oxygen output; particularly noteworthy was its ability to augment the ‘transients’ in bile calcium and bile flow seen immediately after the administration of vasopressin with or without glucagon. T-CDCA, by contrast, produced opposite effects and attenuated all of the parameters measured, and in particular the transients in bile calcium and bile flow. The data provide evidence of a strong correlation between calcium fluxes occurring on both the sinusoidal and the bile-canalicular membranes and that all are modifiable by glucagon, Ca(2+)-mobilizing hormones and bile salts.

Effect of bile salts on bile flow and membrane associated Na-K-ATPase in the perfused rat liver

1995 ◽  
Vol 108 (4) ◽  
pp. A1205
Author(s):  
T. You ◽  
S. Güldütuna ◽  
S. Bhatti ◽  
U. Leuschner
Keyword(s):  
Rat Liver ◽  
Bile Flow ◽  
Bile Salts ◽  
Perfused Rat Liver

Nifedipine modulation of biliary GSH and GSSG/ conjugate efflux in normal and regenerating rat liver

2001 ◽  
Vol 281 (1) ◽  
pp. G85-G94 ◽  
Author(s):  
Bo Yang ◽  
Ceredwyn E. Hill
Keyword(s):  
Bile Acid ◽  
Sodium Nitroprusside ◽  
Rat Liver ◽  
Driving Force ◽  
Bile Flow ◽  
Organic Anion ◽  
High Capacity ◽  
Perfused Rat Liver ◽  
High Affinity ◽  
Glutathione Conjugate Transport

Canalicular glutathione secretion provides the major driving force for bile acid-independent bile flow (BAIF), although the pathways involved are not established. The hypothesis that GSH efflux proceeds by a route functionally distinct from the high-affinity, low-capacity, mrp2-mediated pathway was tested by using perfused rat liver and three choleretic compounds that modify biliary secretion of GSH (the dihydropyridine nifedipine and organic anion probenecid) or GSSG [sodium nitroprusside (SNP)]. Whereas nifedipine (30 μM) stimulated GSH secretion and blocked SNP-stimulated GSSG efflux and choleresis, SNP (1 mM) was ineffective against nifedipine-stimulated GSH efflux or BAIF, suggesting that most GSSG exits through a GSH-inhibitable path independent of high-affinity GSSG/glutathione conjugate transport. Three observations support this proposal. SNP, but not nifedipine, significantly inhibited bromosulfophthalein (BSP, 1 μM) excretion. Probenecid (1 mM) blocked resting or nifedipine-stimulated GSH secretion but only weakly inhibited BSP excretion. Glutathione, but not BSP, efflux capacity was reduced following partial hepatectomy. We suggest GSH efflux is mediated by a high-capacity organic anion pathway capable of GSSG transport when its high-affinity route is saturated.

scholarly journals Cell swelling increases bile flow and taurocholate excretion into bile in isolated perfused rat liver

1992 ◽  
Vol 281 (3) ◽  
pp. 593-595 ◽  
Author(s):  
C Hallbrucker ◽  
F Lang ◽  
W Gerok ◽  
D Häussinger
Keyword(s):  
Bile Acid ◽  
Amino Acid ◽  
Cell Volume ◽  
Rat Liver ◽  
Bile Flow ◽  
Cell Swelling ◽  
Isolated Perfused Rat Liver ◽  
Perfused Rat Liver ◽  
Volume Changes ◽  
Close Relationship

The effects of aniso-osmotically and amino-acid-induced cell-volume changes on bile flow and biliary taurocholate excretion were studied in isolated perfused rat liver. With taurocholate (100 microM) in the influent perfusate, hypo-osmotic exposure (225 mosmol/l) increased taurocholate excretion into bile and bile flow by 42 and 27% respectively, whereas inhibition by 32 and 47% respectively was observed after hyperosmotic (385 mosmol/l) exposure. The effects of aniso-moticity on taurocholate excretion into bile was observed throughout aniso-osmotic exposure, even after completion of volume-regulatory ion fluxes and were fully reversible upon re-exposure to normo-osmotic media. Hypo-osmotic cell swelling (225 mosmol/l) increased the Vmax. of taurocholate translocation from the sinusoidal compartment into bile about 2-fold. Also, cell swelling induced by glutamine and glycine stimulated both bile flow and biliary taurocholate excretion. There was a close relationship between the aniso-osmotically and amino-acid-induced change of cell volume and taurocholate excretion into bile. The data suggest that liver cell volume plays an important role in regulating bile-acid-dependent bile flow and biliary taurocholate excretion.

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