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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.
Thor, P. J. Sendur, R. and Laskiewicz, J.: Effect of stimulation of the vagus nerves and vagotomy on myoelectric activity of small bowel. Acta Physiol. Pol., 1989, 40 (2): 255-261. Experiments have been done on conscious dogs (6 animals) to study vagal 'influences on small bowel motility. First group (3 dogs) was prepared with gastric and esophageal fistulas, the second group (3 dogs) with gastric fistulas. Both groups had mono- polar silver electrodes placed along small bowel. Stimulation of vagus with sham feeding (SF) increased MMC period of about 21°/o. Insulin and 2DG infused intravenously increased MMC period at lower dose Tange and in high doses induced fed-like pattern of motility. Supradiaphragmatic vagotomy done in the second group animals does not change significantly fasted as well as fed motility pattern. These data suggest that central and peripheral vagal input is required for inhibition MMC activity and development fed motility pattern.
This study was designed to determine the role of cholecystokinin (CCK) in postprandial motility pattern of the duodenum and gallbladder (GB) in conscious dogs provided with chronic duodenal electrodes for recording of myoelectric activity and GB fistulas for measurement of intraluminal pressure and volume of GB and to calculate the GB motility index (MI) and GB emptying rate. During naturally occuring activity front (phase III MMC) in the duodenum there was significant increase in the MI of GB accompanied by about 20-30% reduction in the GB volume. These changes in duodenal and GB motility pattern could be duplicated by i. v. motilin. Feeding abolished the appearence of spontaneous activity front in the duodenum and greatly increased motility of GB while reducing its volume. Administration of CCK receptor antagonists in fed dogs failed to affect the motility changes induced by meal in the duodenum but abolished these of the GB. Vagal cholinergic stimulation with insulin, 2DG or urecholine caused similar effects to that induced by food i. e. increased duodenal spike activity, abolished phase III of the MMC, decreased GB volume and increased GB motility. Pretreatment with CCK antagonists did not affect significantly duodenal spike activity or GB motility but significantly increased the GB volume. Atropine 125 µg/kg) blocked almost completely spontaneous activity front in the duodenum and accompanying alterations in the motiliti and volume of GB. We conclude that CCK contributes to the MMC related alterations in the GB motor activity and is essential in cholinergic stimulation induced of the GB emtying but not in vagally induced duodenal and GB motility.
Study was based on hypothesis that electrical stimulation (ES) with parameters obtained from analysis of vagal afferent discharge fed state may fake brain with satiety state. We evaluated effect of denervation of vagal capsaicin-sensitive afferents on food intake and body weight in rats with ES of vagal nerves using microchip (MC). Group A was scheduled to MC implantation, B to sham operation only, C to MC implantation and capsaicin vagal deafferentation, and D to capsaicin denervation only. ES lasted 24 days. MC parameters were 0.05Hz, 0.1s, 0.55V. ES of left vagus significantly reduced total food intake as well as the mean daily intake in groups A and C in comparison to control and D group (ANOVA, F=18.55, p=0.0038). Body weight was lower in group A (346,2 g) and C (272,7 g) then in control (381,4 g) and D (356,8 g) (F=25.68, p=0.00068). Leptin decreased in C (165 pg/mL) in comparison to A (625 pg/mL), B (677 pg/mL), and D (612 pg/mL) (p<0,05), mainly due to ES (F=7.27, p=0.019). Glucose was decreased in A (F=5.55, p=0.036) - by 11 % and by 16% in C group. Proper vagal neuromodulation results in central and peripheral effects causing food intake and body weight downregulation.
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Encoding meal in integrated vagal afferent discharge

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Vagal afferents are integral part of the negative feedback loop induced by constitution and size of food stomach and jejunum. Aim of this study was to assess vagal discharge in response to food and gastric distension in rats. Electrophysiological recordings of vagal afferents in fasted (n=32), fed rats (n=20) and during gastric balloon distension (n=12) were performed. After 60 minutes of fasted nerve recording tube feeding was done. Fasted rats also underwent gastric distension via oesophagus. Vagal afferents discharges were analysed with dual time-amplitude window discriminator. Total vagal afferent discharge in fasted and fed rats revealed 0.3 ± 0.12 vs 0.56 ± 0.22 Hz (p<0.05). We observed two distinct discharge patterns: high amplitude low frequency (HALF) and low amplitude high frequency (LAHF). HALF spikes were observed more frequent in fasted than in fed rats (0.05 ± 0.02 vs. 0.03 ± 0.016 Hz (p<0.05). Conversely LAHF spikes in fed rats predominated over their occurrence in fasted rats: 0.52 ± 0.2 vs. 0.25 ± 0.12 Hz (p<0.05). Left vagal afferents discharge rises with gastric distension of 6, 8 and 10 ml and were: 0.46 ± 0.22 Hz, 0.65 ± 0.31 Hz, 0.86 ± 0.33 Hz (p<0.05) respectively. Similar discharge showed right vagal afferents: 0.41 ± 0.08 Hz, 0.51 ± 0.13 Hz and 0.77 ± 0.27 Hz (p<0.05) for 6, 8 and 10 ml of distension, respectively. We conclude that interdigestive information from gastrointestinal tract is encoded in high amplitude low frequency of spikes pattern in the vagus nerves.
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It is hypothesised that the GABA(B) receptor agonist baclofen increases or has no effect on food intake, and electrical stimulation of vagal nerves decreases food intake. The aim of this study was to evaluate the effects of baclofen in vagally stimulated rats. Material and methods: Thirty two Wistar rats were divided into five groups: group A scheduled for microchip implantation for vagal stimulation, group B for sham operation, group C for microchip implantation and baclofen medication, group D for baclofen medication only and group E for gastric motility evaluation under influence of baclofen. The following parameters were then evaluated: food intake and body mass, gastric motility, leptin, insulin, and glucose serum levels. Results: In the comparison of groups B and A, daily food intake and body weight gain decreased by 17% (p<0.05) and by 22% (p<0.05), respectively. Baclofen alone (group D) did not significantly change either food intake nor diurnal body weight compared to the controls, but when used in conjunction with the microchip (group C) it did significantly reduce effect of vagal neuromodulation (p<0.05). Furthermore, a significant decrease in leptin and glucose levels was detected in group C: 677 to 165 pg/ml (p<0.05) and 5,93 to 4,88 mmol/l (p<0.05), respectively. The administration of baclofen stimulated significantly gastric motility and elicited irregular motor migrating complex (327±200 against control 255±52 cmH2O/s). Conclusions: These results suggest that microchip vagal neuromodulation through increased vagal afferent activity induces an alteration in the feeding behaviour and decreases nocturnal food intake and body weight. These effects were partially attenuated by baclofen. The data suggests that GABA(B) receptors play an important role in the pathomechanism of attenuation of food intake induced by vagal nerve stimulation.
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TENS became widely accepted method of treatment pain syndromes in clinical practice. Lately has been shown that its affects also gastrointestinal tract by releasing NANC neurotransmitter VIP. The aim of this study was to evaluate the effects of TENS on gastric myoelectric activities measured by electrogastrography (EGG). Eighteen healthy men (mean age 23 1.7) were included in the study. Healthy volunteers were divided on 3 groups each 6 persons: with normogastria occurring at 94.5 7% of recording time — group A, with predominant bradygastria (36.6 ± 14%) — group B and with tachygastria (33 14%) — group C. In fasted condition EGG (Synectics, Sweden) was recorded with skin electrodes. TENS 15 min was performed with use of Sinus 5 stimulator (6 Hz, 0.1ms duration, intensities 10 — 20mA, Zimmer, Germany). Stimulating electrodes were placed on non-dominant hand. Results: None of the subjects during TENS reported any side effects or symptoms, during the all studies. In group A in the fasting recordings, after TENS, an decrease of the normal values in the range 2 — 4cpm down to 78.5 ± 21% of recording time (p = 0.03) occurred. The dominant frequency in the bradygastric region increased up to 17.7 7% of the total recording. In group B TENS decreased bradygastria level from 36.6 14% to 20.6 15% (p = 0.02). TENS did not significantly affect tachygastria in group C. Amplitude of the EGG signal after TENS in group B and C increased by 40 and 150% respectively (p < 0.05). Significant decrease of the amplitude was observed in group A (13%). We conclude that TENS by activating centrally mediated somato-visceral reflexes affects gastric electrical activity. Our results suggest that TENS may be useful in treatment of the gastric dysrhythmia.
Food induced neurohumoral signals are conduced to data processing brain centers mainly as vagal afferent discharge resulting in food intake regulation. The aim of this study was to evaluate effects of vagal nerve neuromodulation in control of food intake with fed-pattern microchip (MC) pacing. Experiments were performed on 60 rats divided on 5 groups: I group 0,05Hz left vagal pacing, II - pacing of both vagal nerves with MC 0,05Hz, III- left vagal MC 0,1Hz pacing, IV - pacing of both vagal nerves with MC 0,1 Hz was performed. In group V left vagal pacing was combined with right side abdominal vagotomy. Body weight and total food intake decreased by 12% and 14% (I), 26% and 30%(II), 8% and 21%(III), 14% and 30%(IV), 38% and 41%(IV), respectively (p<0.05). Effects of both vagal nerves stimulation on final body weight and food intake was significantly more effective than only single nerve MC pacing however most effective was stimulation with 0,1Hz combined with right vagotomy. We conclude that vagal stimulation reduce food intake and body weight by increasing vagal afferent signals. Our results suggest that information in vagal afferents can be modulated resulting in changes of feeding behaviour and body weight.
Afferent fibers from gastrointestinal tract outnumber efferents ten times in vagal nerves. Modifying the afferent input makes possible to change discharge of vagal efferents affecting gastrointestinal functions in process known as neuromodulation (NM). Lately it has been used in the treatment of pain and hyperactive neurogenic bladder in urology. MC induced NM may therefore provide a concurrent to pharmacology tool, in treatment of gastrointestinal disorders. The aim of this study was to investigate the effects of long term neuromodulation procedure with use of MC on gastric motility, secretion and weight control in conscious rats. Experiments were performed on 30 Wistar male rats (250—350 g) divided in two groups: sham operated and microsurgically implanted with MC on left vagal nerve below diaphragm. Following stimulation parameters were used: frequency of 0.5—30 Hz, amplitude of 0.55 V, impulse duration of 10 ms in monophasic fashion. In both groups food intake and body weight were measured through the period of 2 weeks after recovery period. Then gastric fistula was implanted in gastric antrum and fasted gastric motility recorded with use of PowerLab system (Australia). Gastric emptying and secretion were also tested with use of phenol red and automatic titration methods. On the daily basis glucose level with standard test and leptin after MC implantation were measured. Recording of vagal activity in fasted rats showed burst of action potentials about 5 ± 2,5 in period of 5000 sec, each burst with spike frequency up to 35 Hz. Food (5 ml of Intralipid – intragastrically) almost doubled amount of bursts to 12 ± 5 in period of 5000 sec with increase in frequency at spike up to 50 Hz. MC induced vagal activity showed continuous spike activity similar to fed pattern. MC induced NM decreases daily food intake by 6% (33.6 ± 4.8 vs control 35.5 ± 4.8 g, p < 0.01). Body weight gain in rats before MC implantation decreased by 20% within 2 weeks after recovery (34.8 ± 9.08 vs control 23.56 ± 4.15 g). Fasting control glucose level also decreased of 5.5% (93.15 ± 9.3 vs control 98.5 ± 11.2 mg%, p < 0.05). Frequency of gastric contractions did not change significantly in MC versus control but amplitude of contractions increased of about 66.7% (2.0 ± 0.8 vs 1.17 ± 0.52) at the dominant frequency 0.08 Hz range and about 71.5% (1.17 ± 0.35 vs 0.68 ± 0.47, p < 0.05) at the frequency 0.12 Hz. in FFT analysis PowerLab (chart v = 4.01). BAO decreased by 29.25% without H+ concentration changes (0.2 ± 0.14 vs 0.14 ± 0.12 mmol/30min, p < 0,05) but MAO did not change in MC rats (0.37 ± 0.25 vs 0.42 ± 0.28 mmol/30min, p0.05). Gastric emptying of isotonic solution increased by 10% (90.46 ± 5.34 vs 80.39 ± 9.95) percent of marker passing to duodenum /5min,.p < 0.0001). Our results suggest that MC induced NM affect brain-gut axis via influencing metabolic and gastric function and decreases body weight. 706
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