<原著>Ethynylestradiolによるラット肝内胆汁うっ滞の作用機序
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It is well known that 17α-ethynylestradiol (EE) causes intrahepatic cholestasis in rats and occasionally in humans although the mechanism has not been fully understood. To elucidate the precise mechanism of EE-induced intrahepatic cholestasis, the relationship between the in vitro changes of taurocholate transport through hepatocyte membrane and the in vivo changes of bile flow after EE treatment was observed and comparisons were made between the control and the EE-treated rats. EE was administered to male SD rats to determine bite flow and biliary bite salt and total bilirubin concentrations, sinusoidal membrane vesicles (SMV) and canalicular membrane vesicles (CMV) of the control and the EE-treated rat liver were isolated and examined for their membrane fluidity, Na^+, K^+-ATPase activity and [^3H]-sodium taurocholate (TC) uptake. Bite flow in the EE-treated rats, in which liver function tests showed cholestatic change, was significantly reduced by 38% from that in the control rats. Bile salt excretion rate was reduced by 38% but total bilirubin excretion rate did not change after EE treatment. Na^+, K^+-ATPase activity of the isolated SMV and CMV did not change although the membrane fluidity in isolated SMV and CMV and the TC uptake in CMV decreased after the EE-treatment. From these results, it is suggested that intrahepatic cholestasis due to EE results from the impairment of Na^+-independent canalicular secretion of bite salts.
- 近畿大学の論文
- 1986-03-25
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