Effect of aspirin on ionic movement and acid hydrolase activity of explants of canine antral and duodenal mucosae.
Lucite chambers, applied to antral and proximal duodenal mucosae with blood supply intact, were used to compare ionic flux and the total, labilized activity of several acid hydrolases including cathepsin D, alpha and beta-galactosidase, beta-N-acetyglucosaminidase, arylsulfatase, and acid phosphatase. Insorption of H+ ion by the antrum is increased by the application of aspirin-acid-salt solution, which also stimulates acid hydrolase activity; acute erosions develop very rapidly. On the other hand, H+ ion is much more rapidly removed from chambers applied to the duodenal mucosa, isolated by the chamber from bile and pancreatic secretions. The same aspirin-acid-salt solution reduces net H+ ion loss from the duodenal chamber, depresses levels of the acid hydrolases, and no ulcers develop.
D000118:Acetylglucosaminidase / Q000378:metabolism; D000135:Acid Phosphatase / Q000378:metabolism; D000818:Animals; D001192:Arylsulfatases / Q000378:metabolism; D001241:Aspirin / Q000494:pharmacology*; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism; D002403:Cathepsins / Q000378:metabolism; D004285:Dogs; D004386:Duodenum / Q000187:drug effects / Q000201:enzymology; D005696:Galactosidases / Q000378:metabolism; D005753:Gastric Mucosa / Q000187:drug effects* / Q000201:enzymology; D006863:Hydrogen-Ion Concentration; D006867:Hydrolases / Q000378:metabolism*; D007413:Intestinal Mucosa / Q000187:drug effects* / Q000201:enzymology; D010437:Peptic Ulcer / Q000139:chemically induced; D011188:Potassium / Q000378:metabolism; D011706:Pyloric Antrum / Q000187:drug effects / Q000201:enzymology; D012964:Sodium / Q000378:metabolism
D012964:Sodium; D006867:Hydrolases; D000135:Acid Phosphatase; D001192:Arylsulfatases; D005696:Galactosidases; D000118:Acetylglucosaminidase; D002403:Cathepsins; D001241:Aspirin; D011188:Potassium; D002118:Calcium