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Postprandial Normal Saline Intake Delays Gastric Emptying of Solids in Conscious Dogs (Partial Involvement of CCK in Its Mechanism)

Abstract

Although it is known that a caloric liquid mealgiven after food intake delays solid gastric emptying,the effect of a noncaloric liquid is not known. The aimsof this study were to determine the effect of normal saline given at 3 hr after feeding ongastric antral motor activity and gastric emptying andto evaluate the role of endogenous cholecystokinin inthe changes in gastric function induced by postprandial saline intake in conscious dogs. Two cannulaswere implanted in each of five mongrel dogs for infusionof phenolsulfonphthalein into the proximal duodenum andfor aspiration of luminal samples from the distal duodenum. Gastric contractile andemptying activity were measured by the force transducermethod and a freeze-drying method newly developed by ourgroup, respectively. Postprandial pancreaticobiliary secretion was assessed from amylase and bileacid outputs into the duodenum. One hundred grams offreeze-dried dog food was given as a solid meal aftermixing it with 100 ml of normal saline. The dogs were given 100 ml of normal saline per os at 3 hrafter feeding. In another study, intravenousadministration of devazepide, a specificcholecystokinin-A receptor antagonist, at a dose of 0.1mg/kg/hr was begun 15 min before postprandial saline intake andcontinued for 1 hr. Gastric antral motility wassignificantly (P < 0.01) inhibited for 30 min afterthe dogs had drunk saline at 3 hr after feeding. Themean fractional emptying rate of gastric solids inpercentage per 30 min after postprandial saline intakewas significantly (P < 0.05) slower than that in thecontrol study without saline intake at 3 hr after feeding. Amylase output into the duodenum afterpostprandial saline intake showed a gradual increaselasting for about 1 hr, whereas that of bile acidincreased transiently but markedly 15 min after saline intake, in comparison with the control study.Pretreatment with devazepide partially ameliorated thesuppression of gastric antral motility. Postprandialintake of saline inhibited gastric motor activity and delayed solid gastric emptying, whereas itincreased the outputs of amylase and bile acid.Endogenous cholecystokinin may be partially involved inthese phenomena caused by saline intake at 3 hr after feeding.

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Tanaka, T., Mizumoto, A., Muramatsu, S. et al. Postprandial Normal Saline Intake Delays Gastric Emptying of Solids in Conscious Dogs (Partial Involvement of CCK in Its Mechanism). Dig Dis Sci 44, 1516–1524 (1999). https://doi.org/10.1023/A:1026642422375

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  • DOI: https://doi.org/10.1023/A:1026642422375

  • FREEZE-DRYING METHOD
  • FORCE TRANSDUCER
  • POSTPRANDIAL AMYLASE OUTPUT
  • POSTPRANDIAL
  • BILE ACID OUTPUT
  • CCK ANTAGONIST