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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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History traces of gastrointestinal motility in Poland

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The objectives of this chapter was to show how motility studies were developed and performed in Poland at the end of century to better understand pathophysiology and improve the clinicians ability to evaluate and treat patients with motility - related disorders. Some of the important historical points along the path to current understanding of the form and function of gastrointestinal motility are presented. Scarce information exists about other than Cracow and Wroc³aw motility centers in Poland in previous century. Lately sophisticated technology became available in Poland and more centers have begun to yield more effective strategies of treatment and enhanced understanding of the pathophysiologic mechanisms underlying GI motility disorders.
The experiments were performed on 3 sheep which had bi-polar platinic electrodes subserously implanted to the uterus shank and horns during an operation. The registration of uterus myoelectrical activity was conducted by the use of Reega Duplex XVI electroencephalograph. The tests were carried out on sheep in uterus, sensitised and non-sensitised with Stilboestrol-Polfa (0.04 mg kg-1 i.m.). After recording the output uterus activity, the sheep were administered serotonin in continuous infusion in the quantity of: 12-24 g kg-1 min-1. The obtained results revealed that serotonin in sheep in anestrus, non-sensitised with stilboestrol, does not cause (within the scope of action potentials) any changes in the electrouterographic record. In sheep sensitised with stilboestrol, serotonin increases the uterus myoelectrical activity.
Experiments were carried out on seven anestrus ewes. The animals were implanted with bipolar electrodes in the horns and corpus uteri. The electrical activity was registered by Reega Duplex electroencephalograph. The experiments were carried out on non-sensitized ewes and ewes sensitized by stilboestrol. The sheep were first fitted with an external jugular vein catheter and histamine (Histaminům hydrochloricum - Polfa) - 3 μg . kg-1 • min-1 - or H1 -receptors blocker (Clemastinum-Polfa) - 50 μg • kg-1 - were introduced. It was found that in sheep sensitized by stilboestrol histamine caused an increase in myoelectrical activity of the uterus by stimulation of H1 - histaminergic receptors.
The research was conducted on 7 inter-breed hybrid sheep, at the age from 10 to 48 months and of the body mass of 32-47 kg, which had bipolar electrodes implanted to the uterus shank and horns. The registration of uterus myoelectrical activity was performed on non-sensitised sheep and 24-48 hours after stilboestrol sensitisation, with the use of electroencephalograph. After recording the output activity, the sheep were administered in continuous infusion: adrenaline – agonist of alpha and beta – adrenergic receptors in the dose of 0.12-0.18 μg ˇ kg-1 ˇ min-1; detomidin – agonist of alpha-adrenergic receptors in the dose of 0.1 – 1.1 μg ˇ kg-1 ˇ min-1; phenylephryn – agonist of alpha1-adrenergic receptors in the dose of 2.1 – 2.9 μg ˇ kg-1 ˇ min-1; xylasine – agonist of alpha2-adrenergic receptors in the dose of 0.5 – 4.0 μg ˇ kg-1 ˇ min-1; prazosin – antagonist of alpha1
The research was conducted on 5 inter-breed hybrid sheep, at the age of 10 to 24 months and of the body mass of 30-45 kg, which had bipolar electrodes implanted to uterus horns and shank. The registration of uterus myoelectric activity was performed on sheep 24 and 48 hours after sensitising with Stilboestrol, by the use of Reega Duplex TR XVI electroencephalograph. After recording the output activity, the sheep were applied intravenously in continuous injection: adrenaline – 0,12-0,18 μg ˇ kg-1 ˇ min-1, oxytocin – 0,25-0,4 i.u., propranolol – 1mg ˇ kg-1, isoprenaline – 0,4-1,5 μg ˇ kg-1 ˇ min-1, salbutamole – 0,4-0,8 μg ˇ kg-1 ˇ min-1. The experiment results are presented in the inclosed drawings. The conducted research revealed that the stimulation of beta-adrenergic receptors causes the decrease or inhibition of uterus myoelectric activity of sheep sensitised with Stilboestrol.
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.
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Electrical activity of canine gallbladder

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Our aims were to describe the myoelectrical activity in the single very thin layer of muscle of the canine gallbladder. The study was performed on 22 freshly removed canine gallbladders. Electrical activity was studied by the single sucrose-gap method and contractility of the tissue was measured simultaneously using a force transducer. The strips (15x1 mm) from different regions of gallbladder (fundus, corpus, neck) were cut in longitudinal, circular and oblique axes. The sucrose-gap apparatus together with connecting tubes, solutions and electrodes were kept at 37°C and the initial tension applied to the tissue was set to 1 g. In 82.7% of recordings, spontaneous myoelectrical activity consisted of regular rhythmic changes in membrane potential similar to slow waves recorded in intestinal tissue. The overall mean frequency was 11.4 ± 5.2 (mean ±SD) cycles per min: 11.1 ± 4.4 cycles per min in fundus, 11.9 ± 6.2 cycles per min in corpus and 10.8 ± 3.8 cycles per min in the neck of the gallbladder. In 84.2% of cases electrical activity correlated with mechanical activity and preceded it. No significant differences were seen between the electrical patterns in strips with different orientations or from the different regions of the gallbladder.
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.
Gastrointestinal dysmotility in Parkinson's disease (PD) has been attributed in part to peripheral neurotoxine action. Our purpose was the evaluation of the salsolinol effect on intramuscular interstitial cells of Cajal (ICC), duodenal myoelectrical activity (DMA) and vagal afferent activity (VAA) in rats with experimental PD. Twenty rats were divided into 2 equal groups. Experimental PD was produced in one group by 3 weeks of the intraperitoneal salsolinol injections (50 mg/kg/day), whereas the 2-nd group served as control. DMA and VAA were recorded in both groups during fasting and stepwise - gastric distension (GD) of 10 ml. Subsequently fragments of duodenum were removed and intramuscular ICC were assessed as c-Kit antigen percentage in the duodenal muscular zone. Analyses of the fasting DMA and VAA recordings didn't reveal differences between the compared groups. During GD increase of DMA dominant frequency (p=0.04) and VAA frequency (p<0.01) was observed in the controls whereas in the salsolinol group both parameters remained unchanged. Image analysis of duodenum revealed decreased c-Kit expression in the salsolinol-injected animals (p=0.05). The results of our study may suggest the direct effect of salsolinol on both ICC and neuronal pathways of gastro-duodenal reflexes.
A long term exposure of the gastric mucosa to inflammatory factors is suspected to alter the normal stomach motility. The consequence of it is an abnormal sensomotor response to food causing dyspeptic symptoms. Our study aimed to investigate the vagal afferents activity and the gastro-duodenal slow wave response to the mild gastric mucosa inflammation in rats. The gastric mucosal inflammation was induced by addition iodoacetamide to drinking water for 5 days. The gastro-duodenal slow wave, vagal nerve recordings and the gastric mucosa examination were performed on 6th day. The iodoacetamide irritated gastric mucosa presented the minimal inflammatory infiltration with mast cells. The vagal afferent activity was significantly increased after iodoacetamide treatment from 0.3 ± 0.1 to 1.9 ± 0.58 Hz, (p<0.05). The gastric slow wave accurate frequencies extracted from the fast Fourier transform spectra accelerated from 0.08 ± 0.01 to 0.1 ± 0.02 Hz (p<0.05). The duodenal frequencies remained unchanged (from 0.64 ± 0.02 to 0.59 ± 0.1 Hz). These results suggest that mild gastric mucosa irritation sensitizes vagal afferents and alters gastric but not duodenal pacemaker activity which may contribute to dyspeptic sensations.
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