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K Sonobe

Publications and source records attributed to K Sonobe.

14 recordsLinked to original sources

Effect of truncal vagotomy on gallbladder bile kinetics in conscious dogs.

Previous studies on the effects of vagotomy on gallbladder (GB) motility have yielded conflicting results. The aim of this study was to evaluate the effects of vagotomy on GB motility and bile kinetics using a new method. Twelve dogs were divided into two groups of six (control and pyloroplasty) and, 4 weeks later, underwent truncal vagotomy. A catheter secured in the GB fundus was used to monitor GB volume. After injecting polyethylene glycol (PEG) into the GB, combined measurements of GB volume and PEG concentration enabled GB emptying and bile kinetics to be estimated. Seven and five of the 12 vagotomized dogs were classified as having large and normal fasting GB volumes, respectively. Postprandial GB emptying was impaired when the fasting GB volume was enlarged. In the fasting state, bile kinetics of vagotomized dogs were significantly smaller than the control values. The emptying ability of the GB of vagotomized dogs with large fasting GB volumes was reduced considerably both in the postprandial and the fasting states. Such retention of bile in the GB after vagotomy may facilitate cholesterol crystal nucleation and stone growth.

Animals↗

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).

Animals↗

Control of gallbladder contractions by cholecystokinin through cholecystokinin-A receptors in the vagal pathway and gallbladder in the dog.

The mechanism of CCK action on gallbladder contractions in the physiological condition is unclear. Gallbladder contractions were monitored by means of chronically implanted force transducers in conscious dogs. Postprandial gallbladder contractions were partially inhibited by atropine and hexamethonium, and completely inhibited by devazepide. In vitro contractile response of canine gallbladder muscle strips to CCK-8 was also studied. CCK-8-induced muscle strip contraction was atropine and tetrodotoxin resistant, but was completely eliminated by devazepide. The existence of CCK receptors in the vagal nerve and gallbladder was examined by means of autoradiography. Forty-eight hours after ligation of the abdominal vagus, CCK-8 binding sites were found to accumulate in the subdiaphragmatic vagal nerve immediately proximal to the ligature, and similar binding sites were also found in the gallbladder smooth muscle layer. These binding sites were displaced by the addition of 10(-7) mol/1 unlabeled CCK-8 and devazepide, but L-365,260 had no effect. In conclusion, it is considerable that postprandial CCK-induced gallbladder contractions are controlled through CCK-A receptors both on the vagal nerve in stimulating endogenous release of acetylcholine and on the gallbladder directly to stimulate muscle contraction in the dog.

Animals↗

Autoradiographic study of motilin binding sites in the rabbit gastrointestinal tract.

Although motilin receptors have been demonstrated by ligand binding studies, there have been no morphological studies of motilin binding site distribution. Light microscopic macro- and micro-autoradiography using highly purified iodinated Tyr23 canine motilin (10(-10) M) was carried out on the gastric antrum, duodenum, cecum and distal colon of the rabbit. Motilin binding sites were found on the smooth muscle layers of the gastric antrum, duodenum and colon, but no positive binding reaction was detected in that of the cecum. Specific binding sites were particularly abundant in the circular muscle layers, with low concentrations in the longitudinal muscle layers of the gastric antrum, duodenum and colon. No motilin binding sites were found in the mucosa of the gastrointestinal tract and pancreas. The intensity of the positive reaction was inhibited when the tissue was incubated with 10(-8) M unlabeled motilin and was completely abolished by 10(-7) M unlabeled motilin. These results are consistent with the difference in contractile response to motilin between the muscle layers of the gastrointestinal tract.

Animals↗