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Introduction and objective. As the autonomic nervous system (ANS) dysfunction is present in course of many disorders, an objective assessment of the ANS function is very important. In practice, the assessment is difficult, and based rather on indirect analysis of autonomically-controlled cardiovascular reflexes, than on direct recording of activity of central or peripheral autonomic structures. The aim of our paper was to discuss briefly current, clinical and scientific ANS investigations, as well as possible future methods of autonomic activity evaluation. A brief description of the state of knowledge. The review presents a short outline of autonomic function assessments based on clinical autonomic tests (e.g. “Ewing’s battery”) and discusses the heart rate variability (HRV) study, as currently popular and widespread option of analysis of the ANS activity. Other, complementary methods, including the baroreceptor sensitivity testing, microneurography or plasma norepinephrine measurement were also mentioned. The article also provides premises related to the determination of selected neuropeptides in plasma or saliva as an innovative concept of autonomic activity assessment. Summary. The available, clinical, non-invasive methods used for assessment of the ANS function are still relatively sparse and, in fact, a surrogate for direct ANS assessment. New methods of autonomic tension determination are still needed that would allow a more complete and reliable assessment. Reports of potential new laboratory markers of the ANS activity (NPY and VIP assay) bring some hope.
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.
In the present study, we examined whether the vagus nerve is involved in mediating the stimulation of hypothalamic-pituitary-adrenal (HPA) axis by cholinergic muscarinic and nicotinic agonists, carbachol and nicotine. The site of HPA axis muscarinic stimulation was determined using peripheral (i.p.) and intracerebroventricular (i.c.v.) administration of carbachol, atropine sulphate (AtrS) and atropine hydrobromide (AtrBr). The i.p. carbachol-(0.5 mg/kg)-induced corticosterone response was significantly reduced by i.p. pretreatment with AtrBr (0.1 mg/kg), but was not diminished by i.c.v. AtrS (0.1µg). The increase in corticosterone secretion induced by i.c.v. carbachol (2 µg) was totally abolished by i.c.v. pretreatment with AtrS (0.1 µg) but was not altered by i.p. AtrBr. Subdiaphragmatic vagotomy performed 2 weeks earlier substantially decreased the i.p. carbachol (0.2 mg/kg)-induced ACTH response and markedly augmented ACTH and corticosterone response to a higher dose of carbachol (0.5 mg/kg) in comparison with the responses in sham operated rats. Vagotomy abolished the stimulatory effect of i.p. nicotine in a low dose (1 mg/kg) on ACTH and corticosterone secretion; the ACTH response to higher dose (2.5 mg/kg) was considerably reduced, while corticosterone response remained unaffected. These results suggest that carbachol given i.c.v. evokes considerable corticosterone response by stimulation of central cholinergic muscarinic receptors. A major part of the i.p. carbachol-induced corticosterone secretion results from peripheral cholinergic muscarinic receptor stimulation. Subdiaphragmatic vagotomy moderately intensified the carbachol-induced ACTH and corticosterone secretion. Vagotomy significantly reduced the nicotine-induced ACTH secretion, possibly by the involvement of vagal afferents. The nicotine-induced corticosterone secretion is not exclusively regulated by circulating ACTH but by various intra-adrenal regulatory components.
Brain histamine participates in central regulation of the hypothalamic-pituitary-adrenal (HPA) axis. Endogenous prostaglandins modulate signal transduction of different neurotransmitters involved in activation of HPA axis. In the present experiment we investigated whether endogenous prostaglandins are involved in the stimulation of ACTH and corticosterone secretion by histaminergic systems in the rat brain. Histamine (50 µg), histamine-trifluoromethyl-toluidine derivative (HTMT, 75 µg) a selective and potent H1-receptor agonist, and amthamine (50 µg) a H2-receptor agonist given intracerebroventricularly (i.c.v.) to non-anesthetized rats considerably increased ACTH and corticosterone secretion 1h after administration. A non-selective cyclooxygenase inhibitor indomethacin (2 mg/kg i.p. or 10 µg i.c.v.), piroxicam (0.02 and 0.2 µg i.c.v.) a more potent antagonist of constitutive cyclooxygenase (COX-1) and compound NS-398 (0.1 and 1.0 µg i.c.v.), a selective inhibitor of inducible cyclooxygenase (COX-2) were given 15 min before histamine and histamine receptor agonists. One hour after the last injection trunk blood from decapitated rats was collected for hormones determination. The histamine-induced ACTH and corticosterone secretion was significantly diminished by piroxicam and was not markedly altered by indomethacin and compound NS-398. The HTMT-elicited increase in ACTH and corticosterone secretion was significantly prevented by indomethacin and was not affected by piroxicam or compound NS-398. The amthamine-evoked increase in ACTH and corticosterone secretion was not markedly influenced by any cyclooxygenase blocker applied in the present experiment. These results indicate that the histamine H1-receptor transmitted central stimulation of the HPA axis is considerably mediated by prostaglandins generated by consititutive cyclooxygenase, whereas stimulation transmitted via H2-receptor does not significantly depend on endogenous prostaglandins mediation.
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Magnetically induced vagus nerve stimulation and feeding behavior in rats

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Vagus nerve (VN) contribute to the bidirectional communication between the gastrointestinal tract and the central nervous system. Stimulation of the VN by a magnetically-driven solenoid with parameters similar to those during food-induced stomach distension has been thought to mimic short-term signaling of satiety and suppress food intake. In this study, the determination of optimal parameters of vagal neuro-modulation to achieve decreased food intake with a resulting reduction in body mass of rats is explored as therapy to treat obesity. The experimental design consisted of three groups of obese adult male Wistar rats: Group 1: VEMF - with solenoid's electrodes placed on the left VN in the magnetic field exposure (MFE); Group 2: EMF - without solenoid's electrodes on the VN in MFE; Group 3: CON - without solenoid's electrodes on the VN outside the MFE. This study suggests that the rats with solenoid's electrodes placed on the left VN significantly decreased their food intake, weight gain and serum leptin concentrations when compared to that of the CON group. PP levels were found to be higher in the VEMF group when compared to the controls groups. It was found that the most effective parameters of vagal stimulation on eating behavior were 3631, 7861, 14523 A2 x h/m2. The magnetic field by unknown mechanisms also influences feeding behavior. This study suggests that vago-vagal reflexes are involved in the feeding homeostasis and that neuromodulation might be an effective method for managing obesity. Further studies are required to confirm these effects in humans.
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