Wyniki wyszukiwania - Biblioteka Nauki

1

Effects of continuous microchip (MC) vagal neuromodulation on gastrointestinal function in rats

100%

Krolczyk G. , Zurowski D. , Sobocki J. , Slowiaczek M. P. , Laskiewicz J. , Matyja A. , Zaraska K. , Zaraska W. , Thor P. J.

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2001

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tom 52

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nr 4,1

EN

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

2

Brain-gut axis in gastrointestinal system: Introductory remarks

86%

Konturek S. J. , Pawlik W. W. , Dajani E. Z.

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nr 4

3-7

3

Visceral sensitivity perturbations integration in the brain-gut axis in functional digestive disorders

86%

Bonaz B.

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nr 4

27-42

EN

Chronic abdominal pain is the most distressing symptom in patients with functionnal digestive disorders (FDD). IBS is the most common gastrointestinal disorder seen in primary care and gastroenterology practice. IBS is a functional bowel disorder in which abdominal pain is associated with defaecation or a change in bowel habit, with features of disordered defecation and with distension. The underlying pathophysiology of IBS is unknown but a chronic visceral hyperalgesia, in the absence of detectable organic disease, is implicated. The exact location of abnormality of visceral pain processing is not known. Theories of its etiology have range widely from the original view that the disease represents a primary disturbance of gut mucosa to emerging conception of the syndrome as emanating from a complex disordered interaction between the digestive and nervous systems. Several lines of evidence suggest a strong modulatory or etiologic role of the central nervous system in the pathophysiology of IBS. A major advance in the understanding of the central mechanisms of pain processing has evolved from application of functional imaging techniques, as represented by positron emission tomography (PET) and functional magnetic resonance imaging (fMRI). In humans, multiple components are involved in somato-visceral pain processings, including sensory-discriminative components, affective components, and cognitive components. Silverman et al, using PET, were the first to explore neural correlates of abdominal pain induced by rectal distension. If healthy subjects activated the ACC, the IBS patients did not while they presented an activation of the left PFC. These findings were consistent with an IBS model that includes both the exaggerated activation of a vigilance network (dorsolateral PFC) and a failure in pain inhibition network anterior cingulate cortex (ACC). In contrast, Mertz et al., using fMRI, observed that pain led to a greater activation of the ACC than did non-painful stimuli thus arguing for an up-regulation of afferent sensitivity to pain. Using fMRI, we also characterized cerebral loci activated by a rectal distension in healthy volunteers. The activation patterns presented a strong similarity with the central processing of somatic pain. In contrast, in a women predominant population of IBS patients, we did not observed any neuronal activation in locations activated in healthy volunteers (ACC, dorsolateral PFC) while a significant deactivation was observed in the IC and in the amygdala, a limbic structure with a role to assign emotional significance to a current experience related to anxiety and fear. Brain imaging techniques thus appear as useful tools to characterize normal and abnormal brain processing of visceral pain in patients with FDD. Reversal effects of chemical compounds targeting these abnormalities either at a peripheral or a central level should be of interest.

4

Inflammatory bowel diseases and brain-gut axis

86%

Hollander D.

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nr 4

183-190

EN

The influence of stress on inflammation in inflammatory bowel disease (IBD) is reviewed. In experimental forms of colitis in rats, stress reactivated the disease. A study of stable IBD patients who were followed for over five years explored the influence of stress on exacerbating the disease. Those patients with high prolonged stressful life events were found to have a 90% recurrence rate of their colitis as compared to only 40% recurrence in low stress patients. Some of the mediators of stress include VIP, TNFalpha, heat shock proteins, glucocorticoid and catecholamines. Stress was shown to increase intestinal permeability to markers such as Cr-EDTA, HRP and dextran 10,000 in rats. In addition, stress increases the permeability of intestinal M-cells. Finally, stress increased the permeability of Paneth cells to HRP. Since Paneth cells synthesize NOD2 mRNA and protein, stress may play a role in the genesis or reactivation of Crohn's disease involving the terminal ileum. Brain-gut interactions via neural, hormonal and cytokine signals can diminish the mucosal protective factors and increase the permeability of luminal antigens into the intestinal epithelial and immune cells. Stress appears to play a key role in exacerbating and accentuating the intestinal inflammation in IBD through brain-gut interactions.

5

Sensory nerves as modulators of intestinal preconditioning

86%

Obuchowicz R. , Pawlik M. , Sendur R. , Szczepanski W. , Biernat J. , Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

6

Central and peripheral neural control of pancreatic exocrine secretion

86%

Niebergall-Roth E. , Singer M. V.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

7

The effect of transcutaneous nerve stimulation [TENS] on gastric electrical activity

86%

Furgala A. , Thor P. J. , Kolasinska-Kloch W. , Kopp B. , Laskiewicz J.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

8

Brain-gut axis and its role in the control of food intake

86%

Konturek S. J. , Konturek J. W. , Pawlik T. , Brzozowski T.

Journal of Physiology and Pharmacology

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2004

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tom 55

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nr 1,2

EN

Gastrointestinal tract (GIT) and nervous system, both central (CNS) and enteric (ENS), are involved in two-way extrinsic communication by parasympathetic and sympathetic nerves, each comprising efferents fibers such as cholinergic and noradrenergic , respectively, and afferent sensory fibers required for gut-brain signaling. Afferent nerves are equipped with numerous sensors at their terminals in the gut related to visceral mechano- chemo- and noci-receptors, whose excitations may trigger a variety of visceral reflexes regulating GIT functions, including the appetitive behaviour. Food intake depends upon various influences from the CNS as well as from the body energy stores (adipocytes) that express and release the product of Ob gene, leptin, in proportion to fat stored and acting in long-term regulation of food intake. Leptin acts through receptors (Ob-R) present in afferent visceral nerves and hypothalamic arcuate nucleus (ARC), whose neurons are capable of expressing and releasing neuropeptide Y (NPY) and agouti related protein (AgRP) that activate the ingestive behaviour through paraventricular nucleus (PVN) (“feeding center”). In addition, to this long-term regulation, a short-term regulation, on meal-to-meal basis, is secured by several gut hormones, such as cholecystokinin (CCK), peptides YY (PYY) and oxyntomodulin (OXM), released from the endocrine intestinal cells and acting via G-protein coupled receptors (GPCR) either on afferent nerves or directly on ARC neurons, which in turn inhibit expression and release of food-intake stimulating NPY and AgRP, thereby inducing satiety through inhibition of PVN. In contrast, during fasting, the GIT, especially oxyntic mucosa, expresses and releases appetite stimulating (orexigenic) factors such as ghrelin and orexins (OX) -A and OX-B, and cannabinoid CB1 agonist. Ghrelin activates growth-hormone secretagogue receptor (GHS-R) in hypothalamic ARC and stimulates growth hormone (GH) release and in vagal afferents to promote the expression and release of hypothalamic NPY and AgRP stimulating PVN and driving ingestive behaviour. The balance and interaction between anorexigenic (CCK, PYY, OXM) and orexigenic (ghrelin and OX) factors originating from GIT appears to play an important role in short-term regulation of food intake and growth hormone (GH) release. An impairment of this balance may result in disorders of feeding behaviour and weight gain (obesity) or weight loss (cachexia).

9

Influence of tianeptine on melatonin homeostasis and psychosomatic symptoms in patients with irritable bowel syndrome

72%

Chojnacki C. , Walecka-Kapica E. , Mokwinska M. , Romanowski M. , Pawlowicz M. , Chojnacki J. , Klupinska G.

Journal of Physiology and Pharmacology

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2013

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tom 64

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nr 2

10

Alteration of peptidergic gut-brain signaling under conditions of obesity

72%

Kuhne S. G. , Stengel A.

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nr 5

11

Effects of continuous microchip [MC] vagal neuromodulation on gastrointestinal function in rats

72%

Thor P. J. , Krolczyk G. , Zurowski D. , Laskiewicz J. , Slawiaczek M. , Matyja A.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

12

The influence of neurotensin and adrenergic system on lipolytic activity in blood and adipose tissue

72%

Piatek J. , Witmanowski H. , Rutkowska D. , Kulinska-Niedziela I. , Paluszak J.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

13

Central action of cholecystokinine antagonists in the intestinal stress induced by duodenal distension in sheep

72%

Kania B. F. , Matczuk J. , Majcher A. , Cieciera M. , Wronska-Fortuna D.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

14

Role of cholinergic receptor subtypes upon the antro-duodenal coordination in sheep

72%

Romanski K. W. , Slawuta P.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

15

Central and peripheral gastroprotective and secretory activity of histamine and its N-alpha methyl analog

72%

Brzozowski T. , Konturek P. C. , Pawlik M. , Kwiecien S. , Pajdo R. , Drozdowicz D. , Konturek S. J. , Hahn E. G.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

16

Leptin is involved in the protective effect of lipopolysaccharide [LPS] in the caerulein-induced pancreatitis

72%

Bonior J. , Jaworek J. , Leja-Szpak A. , Nawrot K. , Kot M. , Bielanski W. , Sendur R. , Pawlik W. W. , Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

17

Sensory neurons and liver protection

72%

Biernat J. , Sendur R. , Obuchowicz R. , Jaworek J. , Zejc-Bajsarowicz M. , Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

18

Effects of biofeedback training on esophageal peristaltis in amyotrophic lateral sclerosis [ALS] patients with dysphagia

72%

Lorens K. , Tomik B. , Pichor A. , Szczudlik A. , Sliwowski Z. , Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

19

The brain-gut axis, functional disturbances after vagotomy

72%

Thor P. J. , Herman R. M.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2

20

Calcitonin increases the inhibitory effect of opioid agonist in guinea-pig ileum

72%

Borowicz B. , Sagan M. , Korzeniowska A.

Journal of Physiology and Pharmacology. Supplement

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2001

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tom 52

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nr 2