Glavin G B, Kiernan K, Hnatowich M R, Labella F S
Eur J Pharmacol. 1986 May 13;124(1-2):121-7. doi: 10.1016/0014-2999(86)90131-7.
The effect of both acute and chronic morphine and naloxone on restraint-stress gastric ulcer formation and on basal gastric acid secretion were examined in the conscious rat. Acute morphine administration produced a dose-related decrease in stress ulceration and basal gastric acid secretion. Acute naloxone treatment resulted in a dose-related increase in stress ulcer formation and markedly augmented gastric acid secretion. Naloxone (4.0 mg/kg) antagonized the ulcer-reducing effects at all doses of morphine tested (4.0-32.0 mg/kg). Morphine-dependent rats, restrained during spontaneous or naloxone-precipitated withdrawal, exhibited the most severe ulceration. However, only those subjected to naloxone-precipitated withdrawal produced a significant increase in gastric acid output. Chronic treatment with naloxone or with chronic naloxone followed by morphine (16.0 mg/kg) resulted in augmented stress ulcer formation relative to all acutely treated groups. Both chronic naloxone-treated groups exhibited markedly enhanced gastric secretion. These data suggest that central and/or peripheral opiate receptors can modulate both basal and stress-perturbed gastric function.
在清醒大鼠中研究了急性和慢性吗啡及纳洛酮对束缚应激性胃溃疡形成和基础胃酸分泌的影响。急性给予吗啡可使应激性溃疡形成和基础胃酸分泌呈剂量依赖性降低。急性给予纳洛酮导致应激性溃疡形成呈剂量依赖性增加,并显著增强胃酸分泌。纳洛酮(4.0毫克/千克)可拮抗所有测试剂量吗啡(4.0 - 32.0毫克/千克)的溃疡减轻作用。吗啡依赖大鼠在自发戒断或纳洛酮诱发的戒断期间受到束缚时,表现出最严重的溃疡形成。然而,只有那些经历纳洛酮诱发戒断的大鼠胃酸分泌显著增加。与所有急性治疗组相比,用纳洛酮慢性治疗或先用纳洛酮慢性治疗后再用吗啡(16.0毫克/千克)治疗,会导致应激性溃疡形成增加。两个慢性纳洛酮治疗组均表现出胃酸分泌明显增强。这些数据表明,中枢和/或外周阿片受体可调节基础和应激干扰的胃功能。