Aspects of the fine structure of the intrahepatic bile duct epithelium in normal and cholecystectomized mice

1968 ◽  
Vol 124 (1) ◽  
pp. 1-21 ◽  
Author(s):  
Kazuyori Yamada
Keyword(s):  
Fine Structure ◽  
Bile Duct ◽  
Intrahepatic Bile Duct ◽  
Duct Epithelium ◽  
Bile Duct Epithelium

Cl−-dependent secretory mechanisms in isolated rat bile duct epithelial units

2001 ◽  
Vol 281 (2) ◽  
pp. G438-G446 ◽  
Author(s):  
Satish K. Singh ◽  
Albert Mennone ◽  
Alessandro Gigliozzi ◽  
Flavia Fraioli ◽  
James L. Boyer
Keyword(s):  
Bile Duct ◽  
Intrahepatic Bile Duct ◽  
Fluid Secretion ◽  
Intracellular Camp ◽  
Camp Concentration ◽  
Uptake Pathway ◽  
Duct Epithelium ◽  
Bile Duct Epithelium ◽  
Rat Bile ◽  
Intracellular Camp Concentration

Cholangiocytes absorb and secrete fluid, modifying primary canalicular bile. In several Cl−-secreting epithelia, Na+-K+-2Cl− cotransport is a basolateral Cl− uptake pathway facilitating apical Cl− secretion. To determine if cholangiocytes possess similar mechanisms independent of CO2/HCO[Formula: see text], we assessed Cl−-dependent secretion in rat liver isolated polarized bile duct units (IBDUs) by using videomicroscopy. Without CO2/HCO[Formula: see text], forskolin (FSK) stimulated secretion entirely dependent on Na+ and Cl−and inhibited by Na+-K+-2Cl−inhibitor bumetanide. Carbonic anhydrase inhibitor ethoxyzolamide had no effect on FSK-stimulated secretion, indicating negligible endogenous CO2/HCO[Formula: see text] transport. In contrast, FSK-stimulated secretion was inhibited ∼85% by K+ channel inhibitor Ba2+ and blocked completely by bumetanide plus Ba2+. IBDU Na+-K+-2Cl− cotransport activity was assessed by recording intracellular pH during NH4Cl exposure. Bumetanide inhibited initial acidification rates due to NH[Formula: see text] entry in the presence and absence of CO2/HCO[Formula: see text]. In contrast, when stimulated by FSK, a 35% increase in Na+-K+-2Cl− cotransport activity occurred without CO2/HCO[Formula: see text]. These data suggest a cellular model of HCO[Formula: see text]-independent secretion in which Na+-K+-2Cl−cotransport maintains high intracellular Cl−concentration. Intracellular cAMP concentration increases activate basolateral K+ conductance, raises apical Cl−permeability, and causes transcellular Cl− movement into the lumen. Polarized IBDU cholangiocytes are capable of vectorial Cl−-dependent fluid secretion independent of HCO[Formula: see text]. Bumetanide-sensitive Na+-K+-2Cl− cotransport, Cl−/HCO[Formula: see text] exchange, and Ba2+-sensitive K+ channels are important components of stimulated fluid secretion in intrahepatic bile duct epithelium.

Proliferation of intrahepatic bile-duct epithelium in biliary atresia

1996 ◽  
Vol 11 (2-3) ◽  
pp. 126-129
Author(s):  
Moazzem Hossain ◽  
Osamu Murahashi ◽  
Hisami Ando ◽  
Kentiro Kaneko ◽  
Takahiro Ito
Keyword(s):  
Bile Duct ◽  
Biliary Atresia ◽  
Intrahepatic Bile Duct ◽  
Duct Epithelium ◽  
Bile Duct Epithelium

scholarly journals A case of primary biliary cirrhosis with thymic hypertrophy and with evidence of HLA-DR2 in peripheral blood and intrahepatic bile duct epithelium.

Kanzo ◽  
1988 ◽  
Vol 29 (10) ◽  
pp. 1397-1403
Author(s):  
Hiroshi SERIZAWA ◽  
Masaya ODA ◽  
Hirokazu KOMATSU ◽  
Akiko IINO ◽  
Kotaro KANEKO ◽  
...  
Keyword(s):  
Bile Duct ◽  
Primary Biliary Cirrhosis ◽  
Peripheral Blood ◽  
Intrahepatic Bile Duct ◽  
Biliary Cirrhosis ◽  
Duct Epithelium ◽  
Bile Duct Epithelium
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