Dimethyl-prostaglandin E2 prevents stress ulceration with minimal complications.

Abstract:

:Gastric mucosal damage produced by topical application of necrotizing agents is diminished by topical or systemic pretreatment with a variety of E and F prostaglandins. The rat restraint model of gastric mucosal injury is more analogous to clinical stress ulceration than are models using intragastric application of toxic solutions; however, previous use of prostaglandin E1 in the restraint model resulted in a prohibitive incidence of GI morbidity. The current study used the restraint model of stress ulceration to compare the effects of a more potent prostaglandin analogue, 16,16-dimethyl prostaglandin E2, with hyperosmolar glucose and antacids. All three agents afforded significant protection from grossly apparent mucosal lesions, alone and in combination. Although other physiologic effects of each agent differed, the only effect which correlated with prevention of mucosal lesions was suppression of gastric acidity. Since effective doses of cytoprotective prostaglandins did not produce notable morbidity in comparison with other agents, they may prove to be a useful adjunct to stress ulcer prophylaxis in clinical settings.

journal_name

Crit Care Med

journal_title

Critical care medicine

authors

Ephgrave KS,Horton J,Burns D

doi

10.1097/00003246-198901000-00011

subject

Has Abstract

pub_date

1989-01-01 00:00:00

pages

53-7

issue

1

eissn

0090-3493

issn

1530-0293

journal_volume

17

pub_type

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