TY - JOUR
T1 - Neural and hormonal mechanisms mediate the enterogastric reflex
T2 - A study in intestinal transplants in rats
AU - Orloff, Susan L.
AU - Bunnett, Nigel W.
AU - Wong, Helen
AU - Walsh, John H.
AU - Debas, Haile T.
N1 - Funding Information:
Received July 31, 1990. Accepted January 29,1991. Address requests for reprints to: Nigel W. Bunnett, Ph.D., Box 0660, Room C-317, University of California, San Francisco, San Francisco, California 94143-0660. Supported by National Institutes of Health grants DK37173 and DK07573. Melissa Balzer assisted in the preparation
PY - 1991/9
Y1 - 1991/9
N2 - To determine the relative contributions of neural reflexes and intestinal hormones to the inhibition of gastric acid secretion by intestinal fat, rats with an extrinsically denervated, transplanted segment of jejunum and those with an innervated segment of jejunum were studied. Postoperatively, meal-stimulated gastric acid secretion was measured by extragastric titration. When secretion reached a plateau, graded doses of oleic acid or saline were instilled into the jejunal segments. In both groups, acid secretion was inhibited by intrajejunal fat but not saline. At doses of 0.4 and 0.08 mmol oleic acid, there was a 25% and 17% greater maximal inhibition of plateau acid response in the innervated rats than in the transplanted rats, presumably because of the neural contribution. To examine the hormonal mediators, the effects of a somatostatin monoclonal antibody and a cholecystokinin A receptor antagonist (L-364,718) on fat-induced inhibition of gastric acid secretion were studied in transplanted rats. Treatment of the patients with transplants with a somatostatin monoclonal antibody (2.18 mg IV) or L-364,718 (1 mg/kg IV) reduced the fat-induced inhibition of acid secretion by 95% and 28%, respectively. In conclusion, both neural and hormonal mechanisms mediate fat-induced inhibition of gastric acid secretion, with the hormonal mechanism predominating. Somatostatin, and to a lesser extent cholecystokinin, contribute to the hormonal mechanism.
AB - To determine the relative contributions of neural reflexes and intestinal hormones to the inhibition of gastric acid secretion by intestinal fat, rats with an extrinsically denervated, transplanted segment of jejunum and those with an innervated segment of jejunum were studied. Postoperatively, meal-stimulated gastric acid secretion was measured by extragastric titration. When secretion reached a plateau, graded doses of oleic acid or saline were instilled into the jejunal segments. In both groups, acid secretion was inhibited by intrajejunal fat but not saline. At doses of 0.4 and 0.08 mmol oleic acid, there was a 25% and 17% greater maximal inhibition of plateau acid response in the innervated rats than in the transplanted rats, presumably because of the neural contribution. To examine the hormonal mediators, the effects of a somatostatin monoclonal antibody and a cholecystokinin A receptor antagonist (L-364,718) on fat-induced inhibition of gastric acid secretion were studied in transplanted rats. Treatment of the patients with transplants with a somatostatin monoclonal antibody (2.18 mg IV) or L-364,718 (1 mg/kg IV) reduced the fat-induced inhibition of acid secretion by 95% and 28%, respectively. In conclusion, both neural and hormonal mechanisms mediate fat-induced inhibition of gastric acid secretion, with the hormonal mechanism predominating. Somatostatin, and to a lesser extent cholecystokinin, contribute to the hormonal mechanism.
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U2 - 10.1016/0016-5085(91)90533-Q
DO - 10.1016/0016-5085(91)90533-Q
M3 - Article
C2 - 1677637
AN - SCOPUS:0025912546
SN - 0016-5085
VL - 101
SP - 734
EP - 742
JO - Gastroenterology
JF - Gastroenterology
IS - 3
ER -