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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.
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Changes of intestinal motility and transit produced by tolerance to and dependence upon morphine have been partly attributed to peripheral mechanisms. We evaluated the effect of chronic peripheral morphine administration and peripheral µ-receptor blockade on vagal afferent activity (VAA) and c-Kit positive intramuscular cells of Cajal (ICCs). Ten rats were subjected to chronic subcutaneous morphine infusion for 72 h with subsequent VAA recording. Potential frequency was evaluated within recordings before and after µ receptor blockade by D-Phe -Cys -Tyr -D-Trp -Orn -Thr -Phe -Thr (CTOP) i.p. injections. Afterwards the rats were sacrificed and intramuscular c-Kit antigen expression was assessed by image analysis within removed fragments of duodenum and ascending colon. An equal group of rats served as a control for VAA and c-Kit expression. Analysis of VAA revealed similar frequencies of potentials in morphine tolerant / dependent rats before CTOP and in the controls. CTOP increased potential frequency in the morphine group which effect was visible mostly within the first 20 minutes (p=0.01). The morphine infused animals presented also higher c-Kit expression in both the duodenum (p<0.001) and the ascending colon (p<0.001) in comparison to the control group. Results of our study may indicate the involment of both the intestinal wall and the long vago-vagal reflexes in tolerance to and dependence upon opioids.
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The effect of orexins on intestinal motility in vitro in fed and fasted rats

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Orexin-A and -B (OXA, OXB) are peptides involved in many gastrointestinal (GI) functions, including motility. Orexins, their precursors and receptors are present in the GI tract. The expression of orexins increases in the hypothalamus and gastrointestinal tract in response to fasting. We have examined the effect of OXA and OXB on GI motility in vitro in fed and fasted rats. The intestinal segments were mounted in chambers filled with Krebs solution. Isotonic contractions were measured in response to acetylcholine (10-5 M), electric field stimulation (EFS), and orexins (10-9-10-7 M) alone or in the presence of orexin-1 type receptor antagonist, SB- 334867 (10-5 M), tetrodotoxin (TTX) 10-6 M, or atropine (10-5 M). Orexins caused a dose-dependent increase of intestinal segment contractions with a more pronounced effect of OXB over OXA. Fasting did not influence orexin-induced responses. Incubation with SB-334867 led to a marked decrease in orexin-induced contractions in OXA-treated segments, while those of OXB were not affected. Atropine diminished contractions only in fasted animals, while TTX led to a decreased response to orexins in both groups. The results show that OXB is predominant in inducing gut motility response, that the effect of orexins is not fully dependent on cholinergic and Na+ transmissions, and that involvement of other transmitters is possible.
Oxidative stress appears to play a role in the pathogenesis of several inflammatory gastrointestinal diseases. Changes in intestinal motility have been reported in different models of intestinal inflammation. The initiating factor of altered motility could be an alteration of gut redox status. The aim of this study was to investigate the effect of oxidative stress evoked by 2, 2´-azobis (2-amidinopropane) dihydrochloride (AAPH) on the intestinal motility of rabbit duodenum and the possible contribution of different K+ channels in mediating this response. Whole thickness segments of rabbit duodenum were suspended in the direction of the longitudinal or circular smooth muscle fibres in an organ bath to study the effects of AAPH alone, or in the presence of different K+ channel blockers on the amplitude, frequency and tone of spontaneous contractions. In circular muscle, AAPH 20 mM induced a reduction of the amplitude, the frequency and tone of the spontaneous contractions. In longitudinal muscle, AAPH 10 mM induced a reduction of the amplitude and tone of the spontaneous contractions. The reduction of the amplitude and tone induced by AAPH was reverted by BaCl2 (1 mM) and TEA (5 mM). Charybdotoxin (100 nM) and iberiotoxin (100 nM) only reverted the reduction of the tone induced by AAPH. In conclusion, our results show that the peroxyl radicals released by AAPH reduced the amplitude and the tone of the spontaneous contractions of the longitudinal smooth muscle from rabbit small intestine. Inward rectifier and intermediate and large-conductance Ca2+-activated K+ channels could be involved in these effects.
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