Berstad K, Vergin H, Postius S, Weberg R, Szelenyi I, Berstad A
Medical Dept., Lovisenberg Hospital, Oslo, Norway.
Scand J Gastroenterol. 1987 Sep;22(7):884-8. doi: 10.3109/00365528708991930.
Suspensions of aluminium hydroxide or a commercial antacid containing aluminium hydroxide (Trigastril) was instilled intragastrically in rats in doses comparable to high and low human therapeutic doses (aluminium hydroxide, 125 mg and 12.5 mg/kg, respectively). Corresponding experiments were carried out with 0.6% citric acid added to the antacid suspensions. Prostaglandin E2 (PGE2) in the gastric content was analysed by radioimmunoassay 6 h after drug administration. Both high and low doses of aluminium hydroxide and Trigastril increased the concentration of PGE2 significantly. Citric acid did not significantly affect the antacid-induced PGE2 release except in combination with a low dose of aluminium hydroxide, with which a significant increase was seen. Release of PGE2 by low doses of antacids implies the possibility that enhanced cytoprotection may be involved in the mechanism by which antacids promote the healing of peptic ulcers.
将氢氧化铝悬液或含氢氧化铝的市售抗酸剂(Trigastril)以与人的高、低治疗剂量相当的剂量(氢氧化铝分别为125毫克/千克和12.5毫克/千克)灌胃给大鼠。在抗酸剂悬液中添加0.6%柠檬酸进行相应实验。给药6小时后,通过放射免疫分析法分析胃内容物中的前列腺素E2(PGE2)。高剂量和低剂量的氢氧化铝以及Trigastril均显著提高了PGE2的浓度。柠檬酸除了与低剂量氢氧化铝联合使用时显著增加PGE2释放外,对抗酸剂诱导的PGE2释放没有显著影响。低剂量抗酸剂引起的PGE2释放意味着增强细胞保护作用可能参与抗酸剂促进消化性溃疡愈合的机制。