Influence of Dehydrocholate on Bilirubin Transport into Bile in the Rat

Abstract

The effect of an intravenous infusion of sodium dehydrocholate on the maximum biliary transport (Tm) of bilirubin was studied in Wistar rats anesthetized with sodium pentobarbitone. Infusion of the synthetic bile salt at 0.24 μmol/min/100 g gave rise to a marked increase in bile flow (69%). The biliary output of taurocholate, phospholipid or cholesterol, compounds which from mixed micelles in bile, was not modified. Neither did the Tm of bilirubin undergo any significant changes, with drops in the bile concentration of the pigment. Our experimental results revealed that bile flow induced by dehydrocholate is not a determining factor of the Tm of bilirubin in the rat.

Influence of Dehydrocholic Acid on the Secretion of Bile Acids and Biliary Lipids in Rats

“…These properties have made this compound useful for physiological studies on bile formation especially when the role of micellar or deter gent properties of the endogenous bile acids is in question [3,7,[10][11][12]21], The data presented in this paper confirm that the high choleretic potential of DHCA is due to the secretion of 3-hydroxy-oxo com pounds. The high choleretic potential of 3-keto-5|3-cholanic acids was shown previously by Dumont et al [22] in rats and Hoffman et al [12] in cats.…”

“…Yousef/Mignault/Weber/Tuchweber retie potential of DHCA [1,2,10,21 ]. These properties have made this compound useful for physiological studies on bile formation especially when the role of micellar or deter gent properties of the endogenous bile acids is in question [3,7,[10][11][12]21], The data presented in this paper confirm that the high choleretic potential of DHCA is due to the secretion of 3-hydroxy-oxo com pounds.…”

“…Rahman and Coleman [26] also reported that when tau rodehydrocholic acid was superimposed with the infusion of taurocholic acid, the time lag between bile acid and biliary lipid output decreased and the increase in biliary lipid secretion became regular and more pronounced. Thus, the inhibition of the bil iary lipid secretion in DHCA infusion must be related to the reduction of the secretion of the endogenous bile acids which was shown previously to be coupled to that of biliary phospholipids secretion [10,[24][25][26][27][28][29][30][31],…”

“…The liver can hydroxylate 7-hydroxycholesterol (5-cholcstene-3p,7a-diol), the precursor of all bile acids mainly in positions 3, 6, 7 and 12, or convert the hydroxyl groups of cholanic acid from one position to another [9]. Thus, it is not surprising that DHCA is con verted mainly to 3a-hydroxylated-oxo bile acids and only small amounts are converted to cholic acid [2][3][4], Infusion of DHCA in rats was shown to reduce the secretion of endogenous bile acids and several investiga tors found no change of biliary lipid secre tion when DHCA was infused in rats, dogs and man, respectively [2,4,6,10,11]. How ever, Hoffman et al [12] showed that infu sion of oxo bile acids in cats resulted in the depression of biliary phospholipid and cho lesterol secretion.…”

Implicación de promotores y transportadores de aniones orgánicos de las familias OATP y ABC en patología, toxicología y terapia antitumoral

“…Por un lado, el ATC, un AB con gran capacidad detergente, no mostró una protección más eficaz que nuestro compuesto. El incremento en el flujo de bilis parece ser más importante que la capacidad de formar micelas, puesto que el ADHC, un AB con escasa capacidad para formar micelas (Gerolami et al, 1972), y por tanto para estimular la secreción biliar de aniones orgánicos, tales como la bilirrubina (Garcia- Marin et al, 1986), ejerció una protección importante frente a la faloidina. Por el contrario, el AUDC, un AB muy colerético (Dumont et al, 1980) y con un buen efecto protector frente al estrés oxidativo inducido por la acumulación de otras especies de ABs durante la colestasis (Perez et al, 2005), mostró un efecto intermedio entre el ATC y el ADHC.…”