Prostaglandin protection against hemorrhage-induced gastric stress ulceration in the rat

• Published in: Digestive diseases and sciences Vol. 34; no. 7; p. 1028
• Main Authors: Ranta-Knuuttila, T, Kiviluoto, T, Hyvärinen, H, Lehtola, A, Kivilaakso, E
• Format: Journal Article
• Language: English
• Published: United States 01.07.1989
• Subjects: 16,16-Dimethylprostaglandin E2 - therapeutic use; Animals; Disease Models, Animal; Hydrogen-Ion Concentration; Prostaglandins E, Synthetic - therapeutic use; Rats; Rats, Inbred Strains; Shock, Hemorrhagic - complications; Stomach Ulcer - etiology; Stomach Ulcer - prevention & control; Stress, Physiological - complications
• ISSN: 0163-2116
• DOI: 10.1007/BF01536369

The present study investigates whether prostaglandins "cytoprotect" the gastric mucosa against hemorrhage-induced stress ulceration by assessing the influence of 16,16-dimethyl prostaglandin E2 (16,16-dm PGE2) on gross and microscopic lesion formation, intramucosal tissue pH, H+ back-diffusion, and mucosal blood flow in rat gastric mucosa exposed to luminal acid (100 mM HCl) during hemorrhagic shock (13 ml/kg for 20 min). Intramucosal tissue pH was measured using pH-sensitive antimony microelectrodes, and mucosal blood flow was measured by the radiolabeled microsphere technique. 16,16-dm PGE2 (5 micrograms/ml topically) significantly protected the gastric mucosa against gross (lesion index 2.25 +/- 0.34 vs 0.87 +/- 0.21) and microscopic (lesion index 2.12 +/- 0.20 vs 0.87 +/- 0.09) damage during the shock. This protection was associated with a significantly lesser acidification of the mucosa during the shock (intramural tissue pH 6.67 +/- 0.08 vs 6.03 +/- 0.17). In order to elucidate whether the lesser intramucosal acidification was due to diminished entry of H+ (H+ back diffusion) into or better disposal of H+ from the mucosa, the influences of 16,16-dm PGE2 on transmucosal H+ fluxes and mucosal blood flow were determined. It appeared that 16,16-dm PGE2 had no influence on the rate of H+ back-diffusion, but it significantly enhanced mucosal blood flow both in the corpus (0.23 +/- 0.04 vs 0.14 +/- 0.03 ml/min/g) and in the antrum (0.24 +/- 0.03 vs. 0.14 +/- 0.03 ml/min/g) during the shock.