AJP - Gastrointestinal and Liver Physiology, Vol 248, Issue 1 20-G27, Copyright © 1985 by American Physiological Society
Effect of acid-base balance and acetazolamide on ursodeoxycholate-induced biliary bicarbonate secretion
J. J. Garcia-Marin, M. Dumont, M. Corbic, G. de Couet and S. Erlinger
Biliary bicarbonate secretion may play an important role in canalicular
bile flow. The aim of this study was to examine the effect of disturbances
in acid-base balance on ursodeoxycholate (UDCA)-induced choleresis and
bicarbonate secretion. Isolated rat livers were perfused with an
erythrocyte-free solution in a recirculating system. In the absence of bile
acid infusion, bicarbonate concentration in bile varied in parallel with
that in the perfusate (15.6-35.1 mM), irrespective of the perfusate pH
(7.26-7.55). Bicarbonate concentration in bile was not significantly
different from that in the perfusate. Under UDCA infusion (2 mumol/min),
bicarbonate concentration in bile and perfusate was correlated (P less than
0.001). Bicarbonate concentration in bile was always higher than that in
the perfusate. Perfusate pH changes (7.25-7.56) induced by changes in
perfusate carbon dioxide tension had no significant effect on bicarbonate
secretion or bile flow. A significant correlation was found between bile
flow and bicarbonate secretion both with and without UDCA. Acetazolamide (1
mM) significantly decreased both UDCA-stimulated bile flow (-27.7%) and
bicarbonate concentration (-51.8%). These results suggest that canalicular
bicarbonate secretion includes an equilibrative component that is possibly
linked to diffusion of plasmatic CO2 or HCO3- and a concentrative transport
that is stimulated by UDCA, is independent of plasma pH, and involves
carbonic anhydrase.
