Aspirin, Prostaglandins and mucopolysaccharide/glycoprotein secretion.
The object of the present study was to investigate the possibility that the ulcer-protective action of prostaglandins (PGs) in eliciting mucus discharge in the stomach could be due to their effect in enhancing the biosynthesis of mucus. Intraperitoneal injection of 2,5 mg/kg PGE2, or the same dose of PGE2 plus 200 mg/kg aspirin (p.o.), both failed to cause any statistically significant changes in the incorporation of radioactive sulphate into gastric mucus glycoproteins in vivo compared with controls. Aspirin, under these conditions, inhibits mucus synthesis in this effect may be related to the development of gastric mucosal damage by this drug. In contrast, PGE2 administration reverses the gastric mucosal damage induced by aspirin so that the ulcer-protective effect of PGE2 appears to be unrelated to mucus synthesis. PGE2 (0.125 - 1.25 microgram/ml) inhibited oxygen consumption and 14CO2 output from 1-14C, and 6-14C glucose in rat gastric mucosal slices in vitro. Thus the absence of effect of PGE2 on mucus biosynthesis may be due to an effect of this PG in reducing the capacity of the mucosa to yield energy (ATP) from the metabolism of glucose.
D000818:Animals; D001241:Aspirin / Q000494:pharmacology*; D005753:Gastric Mucosa / Q000187:drug effects* / Q000378:metabolism; D006023:Glycoproteins / Q000378:metabolism*; D006025:Glycosaminoglycans / Q000378:metabolism; D011453:Prostaglandins / Q000494:pharmacology*; D011458:Prostaglandins E / Q000494:pharmacology; D051381:Rats
D006023:Glycoproteins; D006025:Glycosaminoglycans; D011453:Prostaglandins; D011458:Prostaglandins E; D001241:Aspirin