Ho M M, Ogle C W, Dai S
Eur J Pharmacol. 1986 Jul 15;126(1-2):103-9. doi: 10.1016/0014-2999(86)90744-2.
The effects of morphine, hypoxaemia or hypercapnia on gastric acid secretion, gastric mucus synthesis and the gastric mucosa were studied in conscious rats with pyloric occlusion. Hypoxaemia and hypercapnia were induced by morphine 32 mg/kg given i.p., or each condition was produced separately by adjusting the composition of respired air in the chamber where the animals were kept during the experimental period. Hypoxia significantly enhanced gastric mucus synthesis whereas hypercapnia significantly reduced gastric acid secretion. These effects were significantly alleviated by atropine pretreatment. Morphine-treated rats exhibited decreased gastric acid secretion, increased gastric mucus synthesis and a higher mean ulcer index but only the reduced gastric acid output was significantly prevented by atropine. It is suggested that the effect of morphine on gastric acid secretion may result from its respiratory depressant action and consequent acute stress production. However, the mechanisms by which morphine can increase mucus synthesis and produce ulceration remain obscure.
在幽门闭塞的清醒大鼠中，研究了吗啡、低氧血症或高碳酸血症对胃酸分泌、胃黏液合成及胃黏膜的影响。腹腔注射32mg/kg吗啡可诱导低氧血症和高碳酸血症，或者在实验期间通过调节动物所在实验箱内呼吸空气的成分分别产生这两种情况。低氧显著增强胃黏液合成，而高碳酸血症显著减少胃酸分泌。阿托品预处理可显著减轻这些作用。吗啡处理的大鼠胃酸分泌减少、胃黏液合成增加且平均溃疡指数更高，但只有胃酸分泌减少被阿托品显著抑制。提示吗啡对胃酸分泌的作用可能源于其呼吸抑制作用及随之产生的急性应激。然而，吗啡增加黏液合成及产生溃疡的机制仍不清楚。
