AJP - Gastrointestinal and Liver Physiology, Vol 242, Issue 2 95-G99, Copyright © 1982 by American Physiological Society
Bile acid and bile salt disrupt gastric mucosal barrier in the dog by different mechanisms
W. C. Duane, D. M. Wiegand and C. E. Sievert
The present study was undertaken to assess the mechanism by which
protonated taurocholic acid disrupts the gastric mucosal barrier. By the
criterion of lecithin solubilization, the critical micellar concentration
of taurocholic acid (pH 1) was 4.5 mM, as opposed to 3.0 mM for sodium
taurocholate (pH 7). In canine Heidenhain pouches, taurocholic acid
significantly increased net forward diffusion of Na+ and backdiffusion of
H+ at concentrations of 9, 4.5, and 3.5 mM, indicating that micelle
formation was not required for disruption of the gastric mucosal barrier by
this bile acid. Saturation of the 9 mM taurocholic acid solution with
lecithin (and cholesterol) did not prevent disruption of the gastric
mucosal barrier. At 9 mM, taurocholic acid was absorbed from the pouches at
a mean rate of 1,150 +/- 115 nmol/min in contrast to an absorption rate of
225 +/- 10 nmol/min for sodium taurocholate at the same concentration.
These findings indicate that, unlike ionized bile salts, disruption of the
gastric mucosal barrier by taurocholic acid is mediated largely by uptake
of bile acid by the gastric mucosa rather than dissolution of mucosal
membrane lipids.
