Postprandial normal saline intake delays gastric emptying of solids in conscious dogs: partial involvement of CCK in its mechanism.
Although it is known that a caloric liquid meal given after food intake delays solid gastric emptying, the effect of a noncaloric liquid is not known. The aims of this study were to determine the effect of normal saline given at 3 hr after feeding on gastric antral motor activity and gastric emptying and to evaluate the role of endogenous cholecystokinin in the changes in gastric function induced by postprandial saline intake in conscious dogs. Two cannulas were implanted in each of five mongrel dogs for infusion of phenolsulfonphthalein into the proximal duodenum and for aspiration of luminal samples from the distal duodenum. Gastric contractile and emptying activity were measured by the force transducer method and a freeze-drying method newly developed by our group, respectively. Postprandial pancreaticobiliary secretion was assessed from amylase and bile acid outputs into the duodenum. One hundred grams of freeze-dried dog food was given as a solid meal after mixing it with 100 ml of normal saline. The dogs were given 100 ml of normal saline per os at 3 hr after feeding. In another study, intravenous administration of devazepide, a specific cholecystokinin-A receptor antagonist, at a dose of 0.1 mg/kg/hr was begun 15 min before postprandial saline intake and continued for 1 hr. Gastric antral motility was significantly (P < 0.01) inhibited for 30 min after the dogs had drunk saline at 3 hr after feeding. The mean fractional emptying rate of gastric solids in percentage per 30 min after postprandial saline intake was significantly (P < 0.05) slower than that in the control study without saline intake at 3 hr after feeding. Amylase output into the duodenum after postprandial saline intake showed a gradual increase lasting for about 1 hr, whereas that of bile acid increased transiently but markedly 15 min after saline intake, in comparison with the control study. Pretreatment with devazepide partially ameliorated the suppression of gastric antral motility. Postprandial intake of saline inhibited gastric motor activity and delayed solid gastric emptying, whereas it increased the outputs of amylase and bile acid. Endogenous cholecystokinin may be partially involved in these phenomena caused by saline intake at 3 hr after feeding.
Tanaka
T
T
Gastrointestinal Research Laboratory, Institute for Molecular and Cellular Regulation, Gunma University, Maebashi, Japan.
Mizumoto
A
A
Muramatsu
S
S
Mochiki
E
E
Haga
N
N
Suzuki
H
H
Itoh
Z
Z
D000284:Administration, Oral; D000821:Animal Feed; D000818:Animals; D001647:Bile Acids and Salts / Q000378:metabolism; D002766:Cholecystokinin / Q000502:physiology; D020109:Devazepide / Q000494:pharmacology; D004285:Dogs; D004435:Eating / Q000502:physiology*; D005746:Gastric Emptying / Q000187:drug effects* / Q000502:physiology; D005769:Gastrointestinal Motility / Q000187:drug effects; D006727:Hormone Antagonists / Q000494:pharmacology; D010179:Pancreas / Q000187:drug effects / Q000378:metabolism; D043886:Receptor, Cholecystokinin A; D011949:Receptors, Cholecystokinin / Q000037:antagonists & inhibitors; D012016:Reference Values; D012965:Sodium Chloride / Q000378:metabolism / Q000494:pharmacology*
D001647:Bile Acids and Salts; D006727:Hormone Antagonists; D043886:Receptor, Cholecystokinin A; D011949:Receptors, Cholecystokinin; D012965:Sodium Chloride; D002766:Cholecystokinin; D020109:Devazepide