AJP - Gastrointestinal and Liver Physiology, Vol 248, Issue 3 299-G306, Copyright © 1985 by American Physiological Society
Failure of 16,16-dimethyl PGE2 to prevent inhibitory effect of ethanol on sodium transport in canine gastric mucosa
T. A. Miller, J. M. Henagan, Y. J. Kuo and L. L. Shanbour
By use of an in vitro canine gastric mucosal preparation, we evaluated the
effects of ethanol (2, 4, 6, and 8%, vol/vol) and indomethacin (2.2 X
10(-4)M), with and without 16,16-dimethyl PGE2 pretreatment, on net sodium
transport (JNanet) (mucosal to serosal) across gastric epithelium. Although
administration of 2 or 4% ethanol to the mucosal bathing solution had no
appreciable inhibitory effects on sodium transport, 6 and 8% ethanol and
indomethacin significantly inhibited JNanet when compared with untreated
control mucosa. This effect was accompanied by inhibition of transmucosal
potential difference (PD) and short-circuit current (Isc). In other mucosae
exposed to dimethyl PGE2 (8 X 10(-6) M) in the serosal bathing solution,
significant increases in JNanet, PD, and Isc were noted when compared with
control mucosa. Addition of 6 or 8% ethanol to the mucosal solution of
dimethyl PGE2-pretreated tissue resulted in significant decreases in PD,
Isc, and JNanet below control values that were not significantly different
from mucosa exposed to 6 and 8% ethanol without PG pretreatment. When
indomethacin was added to the mucosal solution following dimethyl PGE2
pretreatment, only slight decreases in PD and Isc below control levels were
observed, and the inhibitory effects on JNanet induced by indomethacin
without such treatment were abolished. These findings suggest that
stimulation of JNanet by prostaglandin may play a role in its ability to
prevent indomethacin damage to gastric epithelium but does not appear to be
of importance in mediating protection against ethanol damage.
