Rees W D, Gibbons L C, Turnberg L A
Scand J Gastroenterol Suppl. 1984;92:63-8.
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.
研究了阿司匹林、吲哚美辛以及前列腺素E2和F2α对离体兔胃黏膜分泌和电活动的影响。在浆膜侧施加吲哚美辛（10⁻⁵ M）或阿司匹林（3×10⁻³ M）可抑制胃底黏膜的碱分泌（平均值±标准误：从0.55±0.06降至0.12±0.06 μmol·cm⁻²·h⁻¹，n = 6，p < 0.01；以及从0.28±0.06降至0.11±0.03 μmol·cm⁻²·h⁻¹，n = 7，p < 0.02）和胃窦黏膜的碱分泌（从0.80±0.03降至0.53±0.21 μmol·cm⁻²·h⁻¹，n = 5，p < 0.01；以及从0.75±0.23降至0.47±0.20 μmol·cm⁻²·h⁻¹，n = 8，p < 0.01）。在黏膜侧和浆膜侧施加前列腺素E2或F2α（10⁻¹⁰至10⁻⁴ M）对胃碱分泌无影响。在浆膜侧施加16,16 - 二甲基E2（10⁻⁶ M）可刺激胃底黏膜的碱分泌（从0.90±0.20增至1.50±0.30 μmol·cm⁻²·h⁻¹，n = 6，p < 0.01），并消除吲哚美辛对胃底和胃窦黏膜碱分泌的抑制作用。16,16 - 二甲基E2预处理并未改变阿司匹林对碱分泌的抑制作用。这些发现表明，阿司匹林和吲哚美辛引起的黏膜损伤可能是通过抑制碱分泌介导的，并且各种前列腺素的保护作用仅部分与对这种分泌的影响有关。
