Protection of gastric mucosa against hypertonic sodium chloride by 16,16-dimethyl prostaglandin E2 or sodium thiosulfate in the rat: Evidence for decreased mucosal penetration of damaging agent

Journal Article · Fri Dec 01 04:00:00 EST 1989 · Digestive Diseases and Sciences; (USA)

DOI:https://doi.org/10.1007/BF01536704· OSTI ID:6984020

Pihan, G; Szabo, S ^[1]

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1. Brigham Women's Hospital, Boston, MA (USA)

Protection of the gastric mucosa may be the result of either increased cellular resistance to injury (cytoprotection) or, alternatively, decreased exposure of mucosal cells to the damaging agent. To determine whether decreased exposure of mucosal cells to damaging agents plays a role in mucosal protection by 16,16-dm PGE2 or sodium thiosulfate, we estimated the intramucosal concentration of 22NaCl and measured its absorption from the gastric lumen into the systemic circulation 1 and 5 min after intragastric administration of hypertonic (25% w/v) 22NaCl. In an attempt to explain the differences observed, we also measured the net transmucosal water flux in control animals and rats pretreated with the protective agents. Administration of hypertonic NaCl rapidly (within 1 min) induced extensive hemorrhagic mucosal lesions that were significantly reduced by pretreatment with 16,16-dm PGE2 or sodium thiosulfate. Ultra-low temperature autoradiography indicated that luminal hypertonic 22NaCl penetrates the upper layers of the mucosa in relatively high concentrations (12.5% w/v) within 1 min but its concentration decreases rapidly and reached low levels (3.12% w/v) by 5 min. Absorption of NaCl from the gastric lumen into the systemic circulation 1 and 5 min after hypertonic NaCl was lower in both pretreatment groups than in the control. Net gastric transmucosal water flux (from serosa to mucosa) increased (P less than 0.05) from 100 +/- 2 in controls, to 1470 +/- 8 and 715 +/- 9 microliters in rats pretreated with 16,16-dm PGE2 and sodium thiosulfate, respectively. We conclude that 16,16-dm PGE2 and sodium thiosulfate protect the gastric mucosa against hypertonic NaCl, diminish mucosal penetration of NaCl, decrease mucosal absorption of NaCl, and significantly increase serosal to mucosal transmucosal water flux.

• OSTI ID: 6984020
• Journal Information: Digestive Diseases and Sciences; (USA), Journal Name: Digestive Diseases and Sciences; (USA) Vol. 34:12; ISSN 0163-2116; ISSN DDSCD
• Country of Publication: United States
• Language: English

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59 BASIC BIOLOGICAL SCIENCES
ABSORPTION
ALKALI METAL COMPOUNDS
ALKALI METAL ISOTOPES
ANIMALS
ANTIOXIDANTS
BETA DECAY RADIOISOTOPES
BETA-PLUS DECAY RADIOISOTOPES
BIOLOGICAL EFFECTS
CHLORIDES
CHLORINE COMPOUNDS
DIGESTIVE SYSTEM
GASTROINTESTINAL TRACT
HALIDES
HALOGEN COMPOUNDS
HEMORRHAGE
INTESTINAL ABSORPTION
ISOMERIC TRANSITION ISOTOPES
ISOTOPE APPLICATIONS
ISOTOPES
LIGHT NUCLEI
MAMMALS
MEMBRANES
MUCOUS MEMBRANES
NUCLEI
ODD-ODD NUCLEI
PATHOLOGICAL CHANGES
PROSTAGLANDINS
RADIOISOTOPES
RATS
RODENTS
SODIUM 22
SODIUM CHLORIDES
SODIUM COMPOUNDS
SODIUM ISOTOPES
SYMPTOMS
THIOSULFATES
TRACER TECHNIQUES
UPTAKE
VERTEBRATES
YEARS LIVING RADIOISOTOPES