Seiji Muramatsu

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 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.

Effect of nitric oxide synthase inhibition on plasma motilin release in fasted dogs

Inhibition of nitric oxide (NO) synthase on plasma motilin concentrations is not known. The aim of this study was to examine the effect of NO synthesis inhibitor on gastrointestinal motility and motilin release in conscious dogs. Dogs fitted with force transducers were given N omega-nitro-L-arginine (L-NNA) after the termination of phase III contractions. Blood samples were taken for measurement of motilin concentrations. L-NNA induced phase III-like contractions in the stomach in the duodenum in association with a significant increase in motilin level. Atropine or hexamethonium significantly inhibited L-NNA-induced phase III-like contractions and the increase in motilin level. Atropine or hexamethonium significantly inhibited L-NNA-induced phase III-like contractions and the increase in motilin level. Ondansetron markedly inhibited gastric, but not duodenal, phase III-like contractions without affecting the increase in motilin level caused by L-NNA. Vagotomy affected neither the occurence of phase III-like contractions nor the increase in motilin level produced by L-NNA. We conclude that inhibition of NO synthesis stimulates motilin release via cholinergic pathways independent of the vagus, and induces phase III-like contractions in the stomach and duodenum. Phase III-like contractions induced by L-NNA are mediated through the activation of 5-HT, receptors.

Relationship Between Gallbladder Bile Concentration and Motility in Conscious Dogs: Role of Cholecystokinin

The relationship between gallbladder (GB) bile concentration and motility was studied in conscious dogs. The 12-h GB bile concentrations between meals could be divided into three periods: diluting, minimum, and concentrating periods. During the diluting period, inhibition of GB contractions by a CCKA receptor antagonist, atropine or hexamethonium, resulted in concentration of GB bile, whereas during the concentrating period, CCK-8 shifted the concentration process back to dilution. The GB appears to absorb water continuously from GB bile, which is not regulated by cholinergic or CCKA receptors. The postprandial progressive dilution of GB bile is brought about by GB pumping controlled by cholecystokinin (CCK).