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EN
Previous studies have indicated that there is a cardiodepressant factor in the medium incubating the posterior pituitary lobe in situ. The cardiodepressant activity of the medium incubating the posterior pituitary lobe before and during stimulation of the vagus nerves was tested on isolated auricles of the right heart atrium of a two-day-old rat. It was found that the medium incubating the posterior pituitary lobe collected before stimulation decreased the contraction rate of the auricle by 34%, while that collected during the intermittent stimulation of the central ends of the cut vagus nerves caused a decrease of the auricle contractions frequency by 52%. The addition of cholinergic, serotoninergic, histaminergic receptor blockers or prostaglandin synthetase into Ringer-Lock’s solution bathing the auricle has no effect on the changes of the contraction rate caused by the incubation medium.
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tom Nr 1
72--89
PL
W artykule przedstawiono rolę narządów zmysłów w powstawaniu zjawiska orientacji i dezorientacji przestrzennej. W wstępnej części autorzy omawiają orientację sytuacyjną (Situational awareness, S.A) oraz zmysły biorące udział w zachowaniu równowagi, a następnie rolę narządu przedsionkowego w omawianych zjawiskach oraz iluzje pochodzenia przedsionkowego.
EN
Respiratory effects of morphine injection to the femoral vein were investigated in urethane and chloralose anaesthetized and spontaneously breathing rats, prior to and after midcervical vagotomy. Bolus injection of morphine HCl at a dose of 2 mg/kg of body weight induced depression of ventilation in all rats, due to the significant decrease in tidal volume and to the decline in respiratory rate both pre- and post-vagotomy. Expiratory apnoea of mean duration of 10.0±3.4 s was present in the vagally intact rats only. Bilateral midcervical section of the vagus nerve precluded the occurrence of apnoea. Prolongation of the expiratory time (TE morphine / TE control), which amounted to10.7±2.2-fold in the intact state, was apparently reduced to 1.5±0.3-fold after division of the vagi. Morphine significantly decreased mean arterial pressure (MAP) at 30 s after the challenge, the effect persisted for not less than 1 minute and was absent in vagotomized rats. The respiratory changes evoked by morphine reverted to the control level after intravenous injection of naloxone at a dose of 1 mg/kg. Results of this study indicate that opioid receptors on vagal afferents are responsible for the occurrence of apnoea and hypotension evoked by morphine.
EN
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.
EN
The aim of our study was to describe anatomical variability of the root entry zone (REZ), also called the Ohersteiner--Redlich zone, that represents the "junction zone" of glia and Schwann sheath of the cranial nerves. This zone has some clinical implications. The pulsatile compression of REZ by a vessel may produce clinical symptoms, such us trigeminal neuralgia, hemifacial spasm, glossopharyngeal neuralgia torticollis spasmodicus or even symptoms of essential hypertension when a vascular crross compression of REZ of a left vagus nerve is present. The vessel - cranial nerve contact in the skull base cysterns may be visualized in radiologic examinations, most accurately in magnetic resonance imaging. Because, we cannot distinguish the REZ from the rest of the vagus nerve in radiologic examinations we decided to measure the lenght of its REZ. The microanatomical study of the lenght of REZ zone of the vagus nerve was performed on 2l nerves taken from 17 human brain stems (12 men, 5 women, 14 left, 7 right), fixed with 8% buffered, formalin solution. Paraffin embedded tissue was cut into 1O-um-thick sections pararellel to the nerve longitudinal axis and stained with hematoxilin & eosin. Each of the nerves showed the presence of a zone of oligodendrocyte myelination, mean lenght 2 ą 0.3 mm. In 17 nerves the transitional zone formred a cone-like process, in 4 nerves was shaped irregularly. The length of REZ (oligodendrocyte myelination plus "glial dome") had the mean length 3.5 ą 0,9 mm.
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Content available remote Luminal CCK and its neuronal action on exocrine pancreatic secretion
84%
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nr 4
81-94
EN
Gut regulatory peptides are produced by mucosal endocrine cells and released both into the circulation as well as into the gut lumen. Following stimulation the distribution between the circulation and gut lumen changes in favor of the gut lumen. In the blood plasma, the biological half-life of gut regulatory peptides is counted in single minutes due to high aminopeptidase activity and liver extraction. In the gut lumen, however, regulatory peptides retain their biological activity much longer, especially in newborn and young animals. A series of studies was performed in neonatal calves and pigs to explore the role of luminal cholecystokinin (CCK) on the regulation of exocrine pancreatic secretion. In anaesthetized neonatal calves, CCK was secreted into the duodenal lumen, and electrical vagal stimulation increased CCK release into the duodenal lumen but not into the circulating blood. In conscious calves, luminal CCK-8 stimulated pancreatic protein secretion by a neurohormonal mechanism dependent on a duodenal mucosal CCK1 receptor and vagal nerve activity. Immunocytochemistry pointed to an association of mucosal CCK1 and CCK2 receptors with neuronal components in the small intestine of neonatal calves. Experiments in calves and pigs with CCK-8 infusions into the duodenal branches of the right gastroepiploic artery confirmed the results of luminal CCK-8 and questioned the physiological relevance of a direct mechanism of CCK on the pancreatic acini.
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Content available remote Short-term depression of inspiratory activity following tonic vagal stimulation
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nr 4
55-61
EN
This study tested the role of inhibitory neurotransmission in the glutaminergic control of short-term depression (STD) of the inspiratory activity initiated by sustained stimulation of the vagus nerve in anesthetized and vagotomized cats. STD, calculated from the integrated phrenic nerve signal, lasted longer when glutaminergic neurotransmission was inhibited by ketamine, a NMDA receptor antagonist. Application of picrotoxin, a GABAA receptor antagonist, reversed the effect of ketamine and shortened the STD duration below that present in the control condition. The results showed that alternation of the neural excitability by antagonists of excitatory and inhibitory neurotransmission modulates the STD of inspiratory activity, evoked by vagal stimulation. The STD depends on the state of neural excitability and is easier accomplished when the excitability is on the high side.
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Content available remote Central and peripheral neural control of pancreatic exocrine secretion
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EN
Efferent vagal impulses act on the exocrine pancreas via pancreatic ganglia, where the impulses are modulated and modified, and terminate via postganglionic fibers at the acinar cells. Acinar muscarinic receptors of the subtype M1 play an important role for the mediation of the stimulatory vagal influences on pancreatic exocrine secretion. In dogs, a potentiative interaction exists between the two most important mediators of the pancreatic exocrine response to intraduodenal stimuli, efferent vagal impulses and CCK. In contrast to humans and rats, in which all action of CCK on pancreatic enzyme output is vagally mediated, CCK acts in dogs in part as a classical humoral factor independent of the cholinergic system. Although several peptides found in pancreatic nerve cell bodies or fibers can stimulate or inhibit pancreatic exocrine secretion, their physiological importance in the neural control of the exocrine pancreas needs to be further evaluated.
EN
Leptin, a product of ob gene controlling food intake, has recently been detected in the stomach and shown to be released by CCK and implicated in gastroprotection against various noxious agents but it is unknown whether centrally applied leptin influences ischemia-reperfusion (I/R)-induced gastric erosions that progress into deeper gastric ulcerations. In this study we compared the effects of leptin and CCK-8 applied intracerebroventricularly (i.c.v.) or intraperitoneally (i.p.) on gastric mucosal lesions induced by I/R and topical application of 75% ethanol. Several major series of Wistar rats were used to examine the effects of leptin and CCK applied centrally on gastroprotection against I/R and ethanol in rats with A) vagotomy by cutting of vagal nerves, B) suppression of NO-synthase with L-NNA (20 mg/kg i.p.), C) inactivation of sensory nerves by capsaicin (125 mg/kg s.c.) and D) inhibition of CGRP receptors with CGRP8-37 (100 µg/kg i.p.) applied with or without the i.c.v. pretreatment with leptin or CCK-8. Rats were anesthetized 1 h after ethanol administration or at 3 h and 3 days upon the end of ischemia to measure the gastric blood flow (GBF) and then to determine the area of gastric lesions by planimetry. Blood was withdrawn for the measurement of plasma leptin and gastrin levels by radioimmunoassay (RIA). Leptin (0.1—20 µg/kg i.p.) dose-dependently attenuated gastric lesions induced by 75% ethanol and I/R; the dose reducing these lesions by 50% (ED50) was 8 µg/kg and 6 µg/kg, respectively and this protective effect was similar to that obtained with CCK-8 applied in a standard dose of 10 µg/kg i.p. This protective effect of leptin was accompanied by a significant increase in GBF and plasma gastrin levels whereas CCK-8 increased plasma leptin levels but failed to affect plasma gastrin levels. Leptin and CCK-8 applied i.c.v. in a dose of 625 ng/rat reduced significantly the area of I/R induced gastric lesions and raised the GBF and plasma leptin levels with the extent similar to those achieved with peripheral administration of leptin or CCK-8 (10 µg/kg i.p.). The protective and hyperemic effects of centrally administered leptin or CCK-8 (625 ng/rat i.c.v.) were completely abolished by vagotomy and significantly attenuated by sensory denervation with capsaicin or by CGRP antagonist, CGRP8-37. The pretreatment with L-NNA to inhibit NO-synthase activity attenuated significantly the protective and hyperemic effects of CCK but not those of leptin while capsaicin denervation counteracted leptin-- induced protection and rise in the GBF but attenuated significantly those of CCK. We conclude that: 1) central leptin exerts a potent gastroprotective activity against I/R-induced gastric erosions that progress into deeper gastric lesions and this protection depends upon vagal activity and sensory nerves and involves hyperemia probably mediated by NO and 2) leptin mimics the gastroprotective effect of CCK and may be implicated in the protective and hyperemic actions of this peptide against mucosal damage evoked by I/R.
EN
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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Content available remote Role of brain-gut axis in healing of gastric ulcers
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EN
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.
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