Publication: Microscopic correlates of adaptive cytoprotection
in an ethanol injury model
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Date
1989
Authors
Schmidt, Carmen L. ; Smith, Gregory S. ; Miller, Thomas A.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
The present study histologically investigated
the efficacy of pretreating rat gastric mucosa with the
mild irritants, 10% and 25% ethanol (EtOH), against the
known damaging effects of 100% EtOH. Fasted rats
received 1 m1 of either water, 10% EtOH, or 25% EtOH
by orogastric intubation. Fifteen minutes later, a portion
of these animals was sacrificed and tissue samples of the
oxyntic region of the stomach were excised and processed
for quantitative histologic analysis. Remaining animals
received a 1 m1 oral bolus of the necrotizing agent, 100%
EtOH. Five minutes later, these animals were sacrificed
and tissues were prepared in a like manner. In a separate
series of experiments, the aforementioned protocols were
repeated, except that al1 animals received the prostaglandin
synthetase inhibitor, indomethacin (5.0 mg/kg intraperitoneally),
30 min before administration of the mild irritant.
Microscopically, the administration of water or 10%
EtOH alone caused a small and comparable amount of
superficial injury to the gastric mucosa. Moreover, both
substances failed to induce protection in stomachs
subseqently exposed to 100% EtOH. Indomethacin
pretreatment did not significantly alter any of these
findings. In marked contrast, 25% EtOH alone elicited a
substantial degree of superficial damage to the gastric
mucosa. Nevertheless it significantly reduced the depth
of injury in animals subsequently challenged by 100%
EtOH. Indomethacin failed to aggravate the effects of
25% EtOH alone, but partially inhibited the protective
effect of this mild irritant against 100% EtOH induced
damage. Our findings indicate that adaptive cytoprotection
is a real phenomenon that can be demonstrated
microscopically. Such protection is limited primarily to
the deep mucosa1 layers (i.e. gastric glands), appears in
part to be prostaglandin mediated and seems to require
the generation of moderate surface cell damage (as occurred with 25% EtOH, but not 10% EtOH) to induce
its initiation.
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