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  • Title: Alkali secretion by isolated rabbit gastric mucosa: effects of non-steroidal anti-inflammatory drugs and prostaglandins.
    Author: Rees WD, Gibbons LC, Turnberg LA.
    Journal: Scand J Gastroenterol Suppl; 1984; 92():63-8. PubMed ID: 6588537.
    Abstract:
    The effects of aspirin, indomethacin and prostaglandins E2 and F2 alpha on the secretory and electrical activity of isolated rabbit gastric mucosa have been studied. Serosal side application of indomethacin (10(-5) M) or aspirin (3 X 10(-3) M) inhibited alkali secretion by fundic mucosa (mean +/- SE: 0.55 +/- 0.06 to 0.12 +/- 0.06 mumol X cm-2 X h-1, n = 6, p less than 0.01 and 0.28 +/- 0.06 to 0.11 +/- 0.03 mumol X cm-2 X h-1, n = 7, p less than 0.02 respectively) and antral mucosa (0.80 +/- 0.03 to 0.53 +/- 0.21 mumol X cm-2 X h-1, n = 5, p less than 0.01 and 0.75 +/- 0.23 to 0.47 +/- 0.20 mumol X cm-2 X h-1, n = 8, p less than 0.01 respectively). Mucosal and serosal side application of prostaglandin E2 or F2 alpha (10(-10) to 10(-4) M) had no effect on gastric alkali secretion. Serosal side 16,16 dimethyl E2 (10(-6) M) stimulated alkali secretion by fundic mucosa (0.90 +/- 0.20 to 1.50 +/- 0.30 mumol X cm-2 X h-1, n = 6, p less than 0.01) and abolished the inhibition of alkali production caused by indomethacin in fundic and antral mucosae. Inhibition of alkali secretion by aspirin was not modified by 16,16 dimethyl E2 pretreatment. The findings suggest that mucosal damage by aspirin and indomethacin may be mediated by inhibition of alkali secretion and that the protective action of various prostaglandins are only partly related to effects on this secretion.
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