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

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.(ABSTRACT TRUNCATED AT 250 WORDS)