Biliary Cef piramide Excretion: Its Relation to Biliary Excretion of Bile Acids and Sulfobromophthalein

Pharmacology ◽  
1995 ◽  
Vol 51 (1) ◽  
pp. 24-32 ◽  
Author(s):  
Hajime Takikawa ◽  
Yoshinobu Uchida ◽  
Naoyo Sano ◽  
Masami Yamanaka
Keyword(s):  
2000 ◽  
Vol 20 (1) ◽  
pp. 38-44 ◽  
Author(s):  
Mitsuhiko Aiso ◽  
Hajime Takikawa ◽  
Masami Yamanaka

2004 ◽  
Vol 39 (10) ◽  
pp. 981-987 ◽  
Author(s):  
Tatsuyuki Marumo ◽  
Toshio Fukusato ◽  
Hajime Takikawa

1956 ◽  
Vol 10 ◽  
pp. 156-157 ◽  
Author(s):  
Sten Eriksson ◽  
Olav Foss ◽  
Ebbe Johansson ◽  
Einar Stenhagen ◽  
B. Thorell

1961 ◽  
Vol 200 (4) ◽  
pp. 855-859 ◽  
Author(s):  
Robert E. Kay ◽  
Cecil Entenman

The rates of excretion of taurocholic acid and lipids in the bile of the isolated perfused liver and the bile fistula rat were determined. In the bile fistula rats, there was, during the first 12 hours after cannulation, a fall in the excretion of taurocholic acid, which was then followed by an increase in the rate of excretion. The excretion of free cholesterol and phospholipids followed the same excretion pattern as for taurocholic acid, whereas the biliary excretion of glycerides and cholesterol esters was nearly constant. Livers perfused immediately after cannulation of the bile duct excreted only very small amounts of bile acids and lipids in the bile. On the other hand, when livers were perfused 48 hours after cannulation, the bile acids were excreted at a greatly accelerated rate and increased amounts of free cholesterol and phospholipids appeared in the bile. The infusion of cholic acid into a liver, perfused immediately after cannulation of the bile duct, gave rise to an increased biliary excretion of bile acids, free cholesterol and phospholipids.


1985 ◽  
Vol 68 (2) ◽  
pp. 127-134 ◽  
Author(s):  
Folkert Kuipers ◽  
Rick Havinga ◽  
Roel J. Vonk

1. Sulphated glycolithocholic acid (SGLC) causes cholestasis in experimental animals, despite its sulphated form. In the present study, the cholestatic potency and the pharmacokinetics of SGLC were investigated in rats under two conditions: (a) in the presence of an intact circulating bile acid pool and (b) after exhaustion of the bile acid pool by 24 h of bile diversion. 2. Intravenous administration of SGLC (8 μmol/ 100 g body weight) to rats with an intact bile acid pool did not cause cholestasis. However, biliary phospholipid and cholesterol concentrations were reduced by 40% and 29% respectively during the first hour after administration. When the same dose of the bile acid was injected in rats with a 24 h biliary drainage, a complete cessation of bile production was observed within 1 h. Twelve hours after the onset of cholestasis, bile production gradually increased again, showed a marked overshoot, and reached control levels after 3 days. In the recovery phase, biliary phospholipid and cholesterol concentrations were greatly reduced. 3. The absence of endogenous bile acids did not change the hepatic clearance rate of a tracer dose of radiolabelled SGLC, but markedly decreased its biliary excretion rate. 4. It was concluded that the hepatotoxic effect of SGLC is much more pronounced in rats with an exhausted bile acid pool, possibly due to a slower biliary excretion of the toxic compound. This phenomenon may have clinical implications for patients with a contracted bile acid pool.


Sign in / Sign up

Export Citation Format

Share Document