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The aim of this study was to examine the influence of cholecystokinin (CCK)-octapeptide (OP) and its amphibian analogue cerulein infusions on duodenal myoelectric and motor activities, as well as to compare the effects of CCK peptides on duodenal bulb and duodenal motility in non-fasted conscious rams. Five rams underwent implantation of bipolar platinum electrodes to the duodenal bulb, and distal duodenum, as well as a strain gauge force transducer near the duodenal electrode. During continuous myoelectrical and motor recordings, 0.15 M NaCl or CCK peptides were administered intravenously. Infusions of CCK-OP at doses of 5 and 50 ng/kg/min and infusions of cerulein at doses of 0.5 and 1.5 ng/kg/min were applied for 60 min and started 15 min after the onset of the duodenal phase 2b of the migrating motor complex. The higher infusion dose of the CCK-OP in the duodenal bulb triggered the strong inhibitory response within few minutes following the start of infusion while in the duodenum its inhibitory effect was shorter and arrived within 40-50 min following the onset of the infusion. The higher dose of cerulein evoked a reaction similar to CCK-OP response in the duodenal bulb while in the duodenum the clear inhibitory response arrived about 20 min earlier than after CCK-OP. A lower infusion dose of CCK peptides evoked less pronounced effects. It is concluded that CCK-OP inhibits ovine duodenal motility in a dose-and region-specific manner. This effect seems to be physiological.
The effect of anticholinergic drugs on gastrointestinal motility is complex and incompletely recognized. Accordingly, in 6 adult sheep bipolar electrodes and strain gage force transducers were surgically attached to the antral, small intestinal and gallbladder wall at the serosal side. During chronic experiments the myoelectric and mechanical recordings were performed in fasted and non-fasted animals before and after various doses of hexamethonium, atropine and pirenzepine given intravenously. Hexamethonium administration triggered rebound excitation after an inhibitory period almost in all the recording sites. Administration of atropine and pirenzepine evoked these secondary contractions mostly in the small intestine and gallbladder. No rebounds were observed when the anticholinergic drugs were given during feeding. In fasted animals, rebound excitation arrived later but more frequently than in non-fasted animals. The excitatory changes were dose-dependent. In the gallbladder, these values were lower than in the small intestine. The frequency of the recurrent pattern was dependent upon the dose of the anticholinergic drug used. It is concluded that nicotinic receptors are more important than muscarinic receptors in the initiation of the rebound excitation in pyloric antrum while in the small bowel and gallbladder the role of both cholinergic receptors is similar. The anticholinergic drugs should be used with caution in all these clinical situations, where the enhancement of gastrointestinal motility must be avoided.
To develop a new animal model for gallbladder ultrasonography 16 adult sheep of both sexes were used. Ultrasonographic examinations were performed in fed or fasted sheep every 30 min for 3-5 h. Every gallbladder was visualized, then its maximal length, height and width were measured. Afterwards, the gallbladder volume was calculated with three methods. The maximal and minimal values of gallbladder volume in both fed and fasted animals differed significantly (p < 0.05) indicating the existence of gallbladder contractions detectable in both states examined. The results of gallbladder volumes calculated with various methods were also significantly different. The values obtained from the method describing the gallbladder as a cone were about 50% lower than that obtained from two ellipsoid methods. The validation study showed that the true value remained somewhere between the values obtained indirectly. This warrants further investigation, however.
Rats, after cannulation of the common bile duct, duodenum and vena cava posterior were infused i.d. with sodium taurocholate to partially maintain the enterohepatic circulation of bile acids. Four-h i.V. infusions of glucagon, Boots secretin, Boots CCK and OP-CCK were continued together with bile acid administration. The bile was collected throughout the experiment and the bile volume, bile acid, phospholipid and cholesterol content in bile were determined. From these results molar lipid per cent and the lithogenic index were computed. During glucagon administration the lithogenic index was enhanced and molar per cent of phospholipids and cholesterol was greater, and that of bile acids was lower, than in rats deprived of hormone infusion. The effect of secretin upon the lithogenic index and the proportion of lipids was similar, although the rate of bile acid secreted was almost twice as high than that during glucagon infusion. When CCK was infused, despite enhanced per cent of bile acids, the lithogenic index was also higher than in the control group. No significant changes in both molar lipid composition and the lithogenic index were obtained when OP-CCK was applied. It is proposed that gastrointestinal hormones can affect bile lithogenicity through alterations of biliary lipid secretion.
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The myoelectric activity of ileum in fasted and fed young pigs

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To precise the character of myoelectric activity of distal small intestine, in 8 young pigs 1 bipolar electrode was attached at the serosal side of the jejunum and 7 electrodes were sutured at terminal ileum. After the recovery, the animals were fed twice daily during at least 2 weeks and were fasted 24 h before each experiment. Myoelectric activity was recorded with electroencephalograph throughout the experiment lasting 3—5 h. After control recording the standard food was given during the end of ileal phase 1 of migrating myoelectric complex (MMC) and registration of myoelectric activity was continued. Ileal propagated or non-propagated minute rhythm was observed in 64% of the experiments performed, during phase 2b of MMC. In most animals studied, the long isolated spike burst series lasting 1—6 min and short isolated spike burst series lasting 15—25 s were observed. Feeding induced myoelectric activity in the jejunum usually after 1—2 min and, in the ileum, during most episodes, after 2—9 min, for 4—10 min. During and after feeding, the short-lasting “transient fed pattern“ was observed. Mean propagation velocity of phase 3 MMC was 4.4 ± 0.8 and 8.1 ± 0.6 cm/min (mean ± S.E.M., p > 0.05) before and after feeding, respectively. Phase 3 MMC was preceded by 2—3 spike burst series lasting 40—70 s each before feeding and 1—3 min after feeding. Single propagated spike bursts arrived more frequently after feeding. Two types of minute rhythm, propagated and stationary, were observed. Giant spike bursts, propagated contractions and ultrarapid spike rushes were recorded occasionally. In conclusion, the myoelectric activity of terminal ileum in swine is eventful, exhibits wide range of irregularity and its response to feeding is relatively weak and delayed as compared to the upper small intestine.
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