Functional cytoprotection by certain antacids.
The effect of different antacids has been investigated on ulcer development, parameters of mucus barrier disruption and gastric PGE2 content in rats. Al(OH)3-containing antacids inhibit gastric ulcer formation induced by alcohol or acetylsalicylic acid (ASA). Changes in parameters of mucus barrier disruption evoked by sodium taurocholate can be significantly diminished by treatment with antacids. This protective effect of antacids is abolished in animals pretreated with indomethacin. PGE2 contents both in gastric mucosa and instillate are increased by pretreatment with antacids. PGE2 content in gastric mucosa or instillate diminished by sodium taurocholate can be normalized by antacid treatment. Although acidic isotonic or acidic hypertonic solutions increase gastric PGE2 content, they are not ulceroprotective. In these solutions, detectable amounts of released PGE2 are minimal. Under in vitro circumstances, the lifetime of PGE2 in gastric juice is shortened by decreasing pH. It has been concluded that Al(OH)3-containing antacids increase PGE2 content in the gastric mucosa. Furthermore, they are capable of lengthening the lifetime of PGE2 in the gastric content. Thus, the clinical use of Al(OH)3-containing antacids in low doses is to be emphasized in the management of gastric ulcer disease.
D000818:Animals; D000863:Antacids / Q000494:pharmacology*; D001241:Aspirin / Q000633:toxicity; D015232:Dinoprostone; D000431:Ethanol / Q000633:toxicity; D005745:Gastric Acidity Determination; D005753:Gastric Mucosa / Q000187:drug effects*; D007213:Indomethacin / Q000494:pharmacology; D008297:Male; D011458:Prostaglandins E / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013276:Stomach Ulcer / Q000139:chemically induced / Q000517:prevention & control*
D000863:Antacids; D011458:Prostaglandins E; D000431:Ethanol; D015232:Dinoprostone; D001241:Aspirin; D007213:Indomethacin