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The present study was undertaken to determine the mechanisms underlying the involvement of upper airway dilating muscles in compensatory responses to added inspiratory resistive load. Experiments were performed in tracheostomized, anaesthetised rabbits. The effect of inspiratory resistive loading on the electromyographic activity of the genioglossus muscle, the major dilating muscle of the pharynx, was studied in vagotomized and vagally intact rabbits during spontaneous breathing with a hypoxic gas mixture (10% O2 in N2) or oxygen. In the vagally intact animals the peak value and duration of genioglossus muscle inspiratory activity increased in the first loaded breath before any noticeable change in the arterial blood gases. Hyperoxia decreased, whereas hypoxia increased the immediate response of the genioglossus activity to inspiratory loading. Removal of vagal volume-related feedback (by vagotomy) significantly increased the genioglossus muscle activity; the increase being more under hypoxia than under hyperoxia. In contrast to vagally intact animals, there was no first-breath increase in genioglossus activity during loading. The results indicate that the immediate involvement of the genioglossus muscle in response to inspiratory resistive load is mediated by vagal-volume feedback. Baseline oxygen tension before loading modulates the immediate reflex vagal-related response of the genioglossus muscle.
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Neural control of the release and action of secretin

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The release and physiological actions of secretin on pancreatic exocrine secretion and gastric secretion of acid and motility are regulated by neuro-hormonal control. The release of secretin by duodenal acidification is mediated by a secretin releasing peptide (SRP). The release and action of SRP are neurally mediated depending on vagal afferent pathway. SRP activity in acid perfusate of the duodenum was substantially decreased when rats were treated with tetradotoxin (TTX), perivagal application of capsaicin, a ß-adrenergic blocker, Met-enkephalin (MEK) or vagotomy. The release of secretin by SRP was abolished in rats treated with TTX, mucosal or perivagal application of capsaicin, MEK or vagotomy. Both release of secretin and pancreatic exocrine secretion (PES) elicited by duodenal acidification were also inhibited dose-dependently by Met-enkepahlin, 5-HT2 antagonist, ketanserin and 5-HT3 antagonist, ondansetron. Stimulation of PES and inhibition of gastric acid secretion and motility by secretin in a physiological dose are also dependent on the vagal afferent pathway as these effects of secretin are abolished by perivagal capsaicin treatment or vagotomy. In conscious rats, vagotomy, vagal ligation, or perivagal colchicine but not capsaicin treatment reduced the number of secretin binding sites in the forestomach suggesting another mode of neural regulation that affects gastric motility. Except in the rat, stimulation of PES by secretin in a physiological dose is profoundly inhibited by atropine indicating the importance of a cholinergic input. In isolated and perfused rat pancreas, electrical field stimulation potentiated secretin-stimulated PES that was suppressed by atropine and anti-GRP serum, suggesting the roles of intrapancreatic cholinergic and GRP-containing neurons. In rats, secretin-stimulated PES was inhibited by a NO synthase inhibitor suggesting mediation by NO. However, the neuropeptides and neurotransmitters involved in regulation of the release and action of secretin and their sites of action remain to be elucidated.
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.
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Role of brain-gut axis in healing of gastric ulcers

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The previous studies demonstrated the pivotal role of capsaicin-sensitive peptidergic sensory neurons and vagal nerves in the maintenance of gastric mucosal integrity. The aim of the present study was: 1) to examine the effect of the functional ablation of sensory neurons with neurotoxic dose of capsaicin and surgical vagotomy on the course of healing of gastric ulcer in rat, and 2) to compare the ulcer healing action of leptin in rats with or without capsaicin-induced inactivation of sensory neurons. Three series of experiments (A, B and C) were performed in Wistar rats with gastric ulcers induced by acetic acid method. In series A, the course of ulcer healing was compared in rats with intact and capsaicin-inactivated sensory neurons. In the series B, the effect of vagotomy on the ulcer healing and accompanying changes in GBF were determined at day 8 and 16 after ulcer induction. The rats of series C, consisting of animals with intact nerves or those with capsaicin-denervation, received the 7-day treatment with exogenous leptin (10 µg/kg i.p. twice daily) to check whether blockade of sensory nerves could influence the acceleration of ulcer healing by this peptide. Capsaicin-induced ablation of sensory neurons significantly delayed ulcer healing and this was accompanied by the significant fall in the GBF and the significant rise in the gastric mucosal gene expression of IL-1ß and TNF-alpha. Vagotomy significantly delayed ulcer healing and led to decrease in GBF at ulcer margin. Treatment with exogenous leptin significantly accelerated ulcer healing, increased the GBF at ulcer margin and upregulated mRNA for iNOS and these effects were attenuated in rats with capsaicin-deactivation of sensory neurons. We conclude that: 1) vagal and sensory neurons contribute to the gastric ulcer healing process possibly due to the increase of GBF, the limitation of inflammatory response, and overexpression of TGFalpha and iNOS resulting in NO release, and 2) the acceleration of ulcer healing by leptin was attenuated in animals with capsaicin-denervation suggesting an involvement of neuropeptides released from sensory afferent nerves in the ulcer healing effect of this hormone.
The effects of an intravenous capsaicin challenge on the respiratory pattern and ventilation were studied in 15 urethane/chloralose-anaesthetized, spontanously breathing rats. Bolus injection of capsaicin at a dose of 5 |Lig/kg into the right femoral vein evoked respiratory arrest in all animals (both prior to and after bilateral midcervical vagotomy), which effect was abolished by ruthenium red pretreatment. Breathing that followed the apnoea was of enlarged tidal volume and initially increased respiratory rate, which resulted in an augmented ventilation. The capsaicin-induced respiratory changes were independent of vagal integrity and may depend on stimulation of vanilloid receptors within the nodose ganglia.
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