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To evaluate the role of endogenous opiates on gastric acid secretion, we infused naloxone, a pure opiate antagonist drug, into 8 healthy subjects in the basal state and then after an amino acid meal. Naloxone significantly reduced basal acid secretion and the gastric acid secretory response to the meal. Maximum inhibition averaged 65% for basal acid secretion and 35% for meal-stimulated secretion. Naloxone had no effect on serum gastrin concentraitons or on the rate of gastric emptying of the meal. In the same subjects morphine also significantly reduced meal-stimulated acid secretion. In contrast to naloxone, morphine delayed gastric emptying and also enhanced the gastrin response to the meal. Morphine also abolished the pancreatic polypeptide response to the meal. Our studies with naloxone suggest that endogenous opiates may augment gastric acid secretion in humans. Failure of exogenous opitates to increase acid secretion suggests that actions other than opiate receptor stimulation (such as anticholinergic effects) may have come into play during morphine infusion.
M Feldman, and
J H Walsh, and
I L Taylor
August 1983,
Gut,
M Feldman, and
J H Walsh, and
I L Taylor
July 1982,
Gastroenterology,
M Feldman, and
J H Walsh, and
I L Taylor
July 1982,
Annals of surgery,
M Feldman, and
J H Walsh, and
I L Taylor
July 1981,
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M Feldman, and
J H Walsh, and
I L Taylor
January 1982,
Gut,
M Feldman, and
J H Walsh, and
I L Taylor
October 1988,
Gastroenterology,
M Feldman, and
J H Walsh, and
I L Taylor
November 1982,
Regulatory peptides,
M Feldman, and
J H Walsh, and
I L Taylor
April 1984,
Archives internationales de physiologie et de biochimie,
M Feldman, and
J H Walsh, and
I L Taylor
October 1991,
Gastroenterology,
M Feldman, and
J H Walsh, and
I L Taylor
September 1979,
Gut,
