Watanabe K, Yano S, Minakawa Y
Department of Drug Evaluation and Toxicological Sciences, Faculty of Pharmaceutical Sciences, Chiba University, Japan.
Eur J Pharmacol. 1987 Nov 17;143(3):293-8. doi: 10.1016/0014-2999(87)90452-3.
The effect of morphine on the gastric acid secretion induced by 2-deoxy-D-glucose (2-DG) was investigated in the perfused stomach of anesthetized rats. The intravenous infusion of morphine (0.01-1.0 mg/kg per h for 2 h) dose dependently suppressed the gastric acid secretion stimulated by 2-DG. This inhibitory effect of morphine was completely reversed by naloxone (1.0 mg/kg i.v.) pretreatment. On the other hand, even the higher dose of morphine (1.0 mg/kg per h for 70 min) had no effect on the gastric acid secretion evoked peripherally by electrical stimulation of the vagus nerve. These observations indicate that morphine suppressed the 2-DG-induced gastric acid secretion via a central mechanism(s), probably mediated by the opiate receptor(s).
在麻醉大鼠的灌流胃中研究了吗啡对2-脱氧-D-葡萄糖(2-DG)诱导的胃酸分泌的影响。静脉输注吗啡(0.01-1.0毫克/千克每小时,持续2小时)剂量依赖性地抑制了2-DG刺激的胃酸分泌。纳洛酮(1.0毫克/千克静脉注射)预处理可完全逆转吗啡的这种抑制作用。另一方面,即使是更高剂量的吗啡(1.0毫克/千克每小时,持续70分钟)对迷走神经电刺激外周诱发的胃酸分泌也没有影响。这些观察结果表明,吗啡通过中枢机制抑制2-DG诱导的胃酸分泌,可能是由阿片受体介导的。