Relevant bibliographies by topics / Ganglions du systeme nerveux autonome

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Academic literature on the topic 'Ganglions du systeme nerveux autonome'

Author: Grafiati
Published: 4 June 2021
Last updated: 15 February 2022

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Journal articles on the topic "Ganglions du systeme nerveux autonome"

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King, B. F., and J. H. Szurszewski. "Peripheral reflex pathways involving abdominal viscera: transmission of impulses through prevertebral ganglia." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 3 (1989): G581—G588. http://dx.doi.org/10.1152/ajpgi.1989.256.3.g581.

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In neurophysiological terms, divergence describes the transmission of impulse traffic from a single afferent line, through an integrating nervous system, and out into multiple efferent lines. This feature has been ascribed to the vertebrate central nervous system and invertebrate ganglionic systems but has not yet been associated with the autonomic nervous system in mammals. Therefore, this study investigated the degree of divergence of afferent impulse traffic through a mammalian autonomic ganglion, the inferior mesenteric ganglion (IMG) in guinea pig. Multiunit discharges were recorded extracellularly from the peripheral nerves, which emerge from the IMG, to determine the lines of efferent outflow (i.e., divergence) of impulse traffic generated by stimulating central efferent and peripheral afferent nerves. Pathways interrupted by a cholinergic ganglion synapse were identified by using hexamethonium. Pathways running directly through the IMG were identified by studying the effects of dividing nerves surgically. A complex arrangement of ascending and descending pathways was revealed, showing a neural network that interconnects the upper gastrointestinal tract, distal colon, and pelvic viscera via prevertebral ganglia.
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Bellezza, M., J. M. Senard, M. Mazerolles, and J. L. Montastruc. "Le Propofol Et Le Pentobarbital Ont -Ils Un Effet Concentration Dependant Sur l'Activite Du Systeme Nerveux Autonome?" Annales Françaises d'Anesthésie et de Réanimation 14 (January 1995): R113. http://dx.doi.org/10.1016/s0750-7658(05)81147-5.

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Orozco, Adriana Vega, Zulema Sosa, Verónica Fillipa, Fabian Mohamed, and Ana María Rastrilla. "The cholinergic influence on the mesenteric ganglion affects the liberation of ovarian steroids and nitric oxide in oestrus day rats: characterization of an ex vivo system." Journal of Endocrinology 191, no. 3 (2006): 587–98. http://dx.doi.org/10.1677/joe.1.06859.

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The axons that constitute the ovarian nervous plexus originate mostly in the principal neurons of the superior mesenteric ganglion (SMG) that is part of the sympathetic ganglionic chain and exhibits cholinergic receptors. In order to observe the effect of acetylcholine, the main neurotransmitter in the ganglionic transmission, the purpose of the present work was: first, to standardize an integrated ex vivo superior mesenteric ganglion-ovarian nervous plexus-ovary (SMG-ONP-O) system in oestrus day rats; secondly, to determine if the ganglionic cholinergic stimulus modifies the release of nitric oxide and steroids in the ovary compartment in the absence of humoral factors; and thirdly, to investigate if there are differences in the responses between the left and right ovaries caused by the neural stimulus. The ex vivo experimental left and right systems were developed and standardized. The systems were incubated in Krebs–Ringer phosphate buffer in a Dubnoff metabolic shaker. The progesterone release was determined to standardize the incubation times, obtaining different responses between the left and right systems, which shows that both systems have their own autonomic tone. Non-specific stimulation with KCl in the ganglion compartment provoked different responses in terms of release of progesterone and oestradiol. Progesterone decreased in the left and right systems. However, oestradiol diminished at short times and increased at 60 and 120 min in the left ovary, whereas it increases at 30 and 60 min in the right ovary. These different responses show the sensitivity and viability of both systems. When acetylcholine was used in the ganglion compartment, the release of nitric oxide, progesterone, androstenedione and oestradiol was evaluated. The liberation of nitrite increased at 15, 30 and 60 min in the left system and decreased in the right system at 120 min. Progesterone showed a decrease in its release at 15, 30 and 120 min and androstenedione at 15 min in the left ovary compartment. In the right ovary, only progesterone decreased in relation to the control at 120 min while androstenedione did not show significant changes. Oestradiol showed an increase in the left ovary compartment at all the studied times, while in the right ovary it did not show any changes. These results indicate that the neural stimulus from the superior mesenteric ganglion through the ovarian nervous plexus is one of the factors modulating the secretory activity of the ovarian steroids and nitric oxide. The system is viable and also shows a different sensitivity of the left ovary in relation to the right one at least in this cycle stage, characterized by marked irrigation and profound structural changes in the ovary.
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Zubicki, A., L. Sels, V. Safa, et al. "Effets Sur l'Hemodynamique Et Sur Le Systeme Nerveux Autonome Du Desflurane Administre Avec Du Protoxyde d'Azote Chez Les Operes De Chirurgie Vasculaire." Annales Françaises d'Anesthésie et de Réanimation 14 (January 1995): R155. http://dx.doi.org/10.1016/s0750-7658(05)81189-x.

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Kelash, Fnu, Lara Kujtan, and Padmaja V. Mallidi. "Acroparesthesia in a Female: Diagnostic Dilemma." Case Reports in Medicine 2014 (2014): 1–2. http://dx.doi.org/10.1155/2014/172197.

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Fabry disease is an X-linked lysosomal storage disorder caused by deficient activity of a-galactosidase A (also known as ceramide trihexosidase) and resultant accumulation of globotriaosylceramide (Gb3) and related glycophospholipids. The disease affects nearly all major organ systems, with the primary sites damaged by Gb3 including renal glomeruli, myocardium, neurons of the dorsal ganglion and autonomic nervous system, and vascular endothelial and smooth muscle. Progressive deposition in these organ systems leads to renal and heart failure; debilitating pain as a result of nervous system involvement also occurs.
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Hambræus, Johan, and Hans Westergren. "Treatment of post-traumatic pain, and autonomic and muscular dysfunction by ganglion impar block and medial branch block of the facet joints: A case report." Scandinavian Journal of Pain 3, no. 4 (2012): 228–40. http://dx.doi.org/10.1016/j.sjpain.2012.07.002.

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AbstractIntroductionPatients exposed to whiplash trauma are at risk of developing pain and dysfunction of the neck and shoulder. Although rarely discussed in the literature, some patients also develop autonomic dysfunction.Case presentationA previously healthy 41-year-old woman was involved in a “head-on” car crash. During the following 3 years she developed severe and complex post-traumatic pain syndrome, which consisted of neck pain, lumbar pain, sensory-motor dysfunction, and myoclonic muscular contractions. Despite pharmacotherapy, physiotherapy, and rehabilitation, her condition worsened, resulting in severe disability. Fourteen years after the car crash, an interventional pain therapy program was started, which consisted of sympathetic ganglion impar block and medial branch blocks of facet joints at different levels. These treatment strategies ultimately normalized her sensory-motor dysfunction, reduced her autonomic dysfunction, and stopped the myoclonic muscular contractions.ConclusionThis case highlights a possible interaction between the pain-generating facet joints, the somatosensory nervous system, and the autonomic/sympathetic nervous systems. The case also highlights the importance of identifying autonomic dysfunction in patients with persisting pain syndromes.ImplicationsThis complex case shows that many clinical phenomena cannot be explained using our present knowledge of pain mechanisms. We hope that readers who have observed similar cases can learn from our case, and are encouraged to publish their observations.
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Tumanov, V. "Діазинон. Основні аспекти біологічної дії, токсикологічні властивості та патоморфологія отруєнь". Scientific Messenger of LNU of Veterinary Medicine and Biotechnologies 19, № 77 (2017): 131–36. http://dx.doi.org/10.15421/nvlvet7729.

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The article represents data on chemical properties and main aspects of the biological action of the diazinon - organophosphate pesticide that is widely used as a drug with marked acaricidal and insecticidal properties. Analyzed published data on metabolism, diazinon accumulation in various organs and systems, and ways of removing from the body. The article shows the median lethal dose (LD50) diazinon for various kinds of animals. The special features of the pathogenesis of poisoning, the main mechanism of action of toxic organophosphorus pesticides is the phosphorylation and inhibition of acetylcholinesterase, resulting in a marked accumulation of acetylcholine in the cholinergic synapses, excessive stimulation of nerves and muscles, disruption passage of nerve impulses. The article detailed the clinical signs of acute poisoning by organophosphate compounds. These data indicate that the effects on the body organophosphorus pesticides includes muscarinic effects (sialorrhea and excessive secretion of sweat glands, bronchorrhea, increased motility of the gastrointestinal tract, accompanied by spastic contractions of the intestinal wall, vomiting and gastroenteritis), nicotine action (miofibrillation, rigidity pectoral muscles, paralysis of respiratory muscles with the development of sudden hypoxemia) and central effects (arising from the impact of the central nervous system and are accompanied by violation of its function). The analysis pathmorphology of poisoning of the organophosphate pesticide. These data indicate that structural changes diazinon poisoning is less specific than clinical signs and characterized by: the development of the circulatory disorders (acute congestive hyperemia recorded and hemorrhage), the appearance of dystrophic and necrotic changes parenchymal elements of the brain and spinal cord, liver, kidneys and so on. Also recorded alterations changes ganglion cells and spinal cord autonomic ganglion, proliferation of glial cells, and for subacute and chronic poisoning – disintegration of the myelin and nerve fibers axial cylinder. Described diazinon influence on organs of the immune system and ability to induce endocrine disorders. There are published data on the potential mutagenic, carcinogenic and teratogenic effects of the diazinon. The range of problems researd structural changes by the origin and development of clinical evidence for the effect of different doses diazinon and certain aspects of forensic veterinary diagnostic poisoning mammals and birds of organophosphate pesticides.
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Brand, P. H., P. J. Metting, and S. L. Britton. "Support of arterial blood pressure by major pressor systems in conscious dogs." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 3 (1988): H483—H491. http://dx.doi.org/10.1152/ajpheart.1988.255.3.h483.

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The roles of the autonomic nervous system, vasopressin, and angiotensin II in support of blood pressure were evaluated in seven conscious, resting dogs while hydrated or dehydrated. Mean arterial blood pressure (MAP) was monitored, and the dogs were given hexamethonium to block autonomic ganglia. Thirty minutes later, they were given captopril, and after another 30 min, a vasopressin V1 antagonist, d(CH2)5TyrMeAVP, was given. The order okf administration of captopril and d(CH2)5TyrMeAVP was alternated in different experiments. Hexamethonium had no effect on steady-state MAP in either hydrated or dehydrated dogs. In hydrated dogs, the average MAP was 100 mmHg; d(CH2)5TyrMeAVP decreased MAP by approximately 12 mmHg, and captopril decreased MAP by 24 mmHg. The magnitude of the effect of these two inhibitors was independent of the order of their administration. Dehydration doubled the effect of d(CH2)5TyrMeAVP on MAP but had no effect on the response to captopril. The results suggest that 1) autonomic function is not essential for maintenance of arterial blood pressure in resting dogs; 2) during autonomic ganglionic blockade, arterial blood pressure is supported by both angiotensin II and vasopressin; and 3) dehydration increases the role of vasopressin in control of blood pressure.
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Kamiya, Yoshinori, Tomio Andoh, Itaru Watanabe, Tomoko Higashi, and Hideki Itoh. "Inhibitory Effects of Barbiturates on Nicotinic Acetylcholine Receptors in Rat Central Nervous System Neurons." Anesthesiology 94, no. 4 (2001): 694–704. http://dx.doi.org/10.1097/00000542-200104000-00025.

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Background Neuronal nicotinic acetylcholine receptors (nAChRs) are widely expressed in the central and autonomic nervous systems. The authors have previously shown that depressant and convulsant barbiturates both inhibit the ganglion-type nAchRs in PC12 cells. However, the central and gangliontype receptors have different subunit composition and pharmacologic properties. In this study, the authors investigated the effects of thiopental, depressant [R(-)] and convulsant [S(+)] stereoisomers of 1-methyl-5 phenyl-5-propyl barbituric acid (MPPB) on neuronal nAChRs in the rat central nervous system to explore significance of these effects in barbiturate anesthesia. Methods Whole-cell currents were measured in acutely dissociated rat medial habenula (MHb) neurons by applying 10 or 100 microM nicotine in the absence or presence of thiopental 3-100 microM. Effects of R(-)- and S(+)-MPPB on the nicotine-induced current were also studied. Results Thiopental suppressed the nicotine-elicited inward current and accelerated the current decay dose-dependently at the clinical relevant concentrations. R(-)- and S(+)-MPPB both inhibited the nicotine-induced current dose-dependently without augmenting the current decay. There was no significant difference in the magnitudes of inhibition by R(-)- and S(+)-MPPB. Conclusions Although thiopental suppressed the current mediated through native nAchRs in rat MHb neurons at the clinically relevant concentrations, the depressant and convulsant stereoisomers of MPPB both inhibited the current in the same extent. These findings are consistent with the results previously obtained in the ganglion-type receptors of PC12 cells and suggest that inhibition of nAChRs in MHb neurons is not directly relevant to the hypnotic or anticonvulsive actions of barbiturates.
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Greeley, G. H., F. Lluis, G. Gomez, J. Ishizuka, B. Holland, and J. C. Thompson. "Peptide YY antagonizes beta-adrenergic-stimulated release of insulin in dogs." American Journal of Physiology-Endocrinology and Metabolism 254, no. 4 (1988): E513—E517. http://dx.doi.org/10.1152/ajpendo.1988.254.4.e513.

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Peptide YY (PYY) and neuropeptide Y (NPY) are peptides of 36 amino acids that share structural homologies with pancreatic polypeptide (PP). PP is predominantly found in the endocrine pancreas. PPY is primarily found in mucosal endocrine cells of the distal ileum, colon, and rectum, whereas NPY is found in both the peripheral and central nervous systems. Previous studies indicate that these peptides can interact with the autonomic nervous system. The objective of the present experiments was to study the effect of PYY on neurally stimulated insulin release [i.e., in response to 2-deoxy-D-glucose (2-DG), a nonmetabolizable glucose analogue] in conscious dogs. Intravenous administration of PYY (100, 200, and 400 pmol.kg-1.h-1) reduced 2-DG-stimulated insulin release in a dose-dependent manner (P less than 0.05) without affecting plasma glucose levels. Administration of NPY (800 pmol.kg-1.h-1), but not PP (400 pmol.kg-1.h-1), reduced 2-DG-stimulated release of insulin (P less than 0.05). The inhibitory action of PYY on 2-DG-stimulated insulin release persisted in the presence of atropine or phentolamine treatment; however, hexamethonium alone or phentolamine plus propranolol treatment blocked the inhibitory action of PYY. Release of insulin stimulated by the beta-agonist isoproterenol was also inhibited by PYY (P less than 0.05). These results indicate that PYY can inhibit autonomic neurotransmission by a mechanism that may involve ganglionic or postganglionic inhibition of beta-adrenergic stimulation. Our findings suggest a role for PYY and NPY in the autonomic regulation of insulin release.
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Dissertations / Theses on the topic "Ganglions du systeme nerveux autonome"

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Hamel, Olivier Robert Roger. "Ganglions végétatifs céphaliques anatomie descriptive, topographique et fonctionnelle; intérêts cliniques. /." [S.l.] : [s.n.], 2004. http://theses.univ-nantes.fr/thesemed/SPEhamel.pdf.

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Xue, Zhi-Gang. "Recherches sur la différenciation du système nerveux periphérique chez les oiseaux : mise en évidence et propriétés des précurseurs de type autonome présents dans les ganglions sensoriels." Paris 13, 1987. http://www.theses.fr/1987PA132008.

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Dimitriadou, Violetta. "Donnees anatomophysiologiques en faveur d'un role non vasomoteur de l'innervation autonome des vaisseaux cerebraux : role trophique au cours du developpement et de l'age adulte, possibilite d'une intervention indirecte parl'intermediaire de cellules." Paris 6, 1988. http://www.theses.fr/1988PA066200.

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Xue, Zhi-Gang. "Recherches sur la différenciation du système nerveux périphérique chez les oiseaux mise en évidence et propriétés des précurseurs de type autonome présents dans les ganglions sensoriels /." Grenoble 2 : ANRT, 1987. http://catalogue.bnf.fr/ark:/12148/cb37610856d.

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Toussirot, Éric. "L'atteinte du systeme autonome dans la polyarthrite rhumatoide : etude de 40 cas." Aix-Marseille 2, 1991. http://www.theses.fr/1991AIX20814.

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RAMMELOO, BENEDICTE. "Acupuncture et modifications du systeme nerveux autonome au cours d'une serie d'epreuves anxiogenes." Lyon 1, 1988. http://www.theses.fr/1988LYO1M241.

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SCHUMANN, MUHAMMAD AHMAD. "ELECTROPHYSIOLOGICAL ANALYSIS OF CHOLECYSTOKININ ACTIONS IN MAMMALIAN INFERIOR MESENTERIC GANGLION (AUTONOMIC REFLEX)." Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183872.

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Cholecystokinin (CCK)-like immunoreactive materials have been localized in neurons with cell bodies in the colon and axons in the IMG of the guinea pig. The physiological significance of neuronal CCK in sympathetic prevertebral ganglia is unknown. The goal of the present studies is to test the hypothesis the CCK is a neurotransmitter in the IMG of guinea pig and rabbit. In vitro IMG preparations with or without a segment of the colon attached were utilized to conduct intracellular recordings of potentials elicited in the neurons by pressure-ejected CCK₈. The peptide triggered a depolarization with rapid onset (1-5 s) and a rate of rise (1.6 ± 0.4 mV/s) in 95% of the neurons tested. Values of the ED₅₀ for effecting depolarization average 1.1 ± 0.5 pmoles. In 59% of the cells, the depolarization was associated with a decrease in R(in) and in 20% with an increase. The remaining cells showed no change in R(in). G(Na) and G(K) were increased and decreased, respectively; potential-dependence characteristics revealed a null potential of 36 ± 9 mV in those cells exhibiting a decrease in R(in). Gastrin, caerulein, and CCK₂₇₋₃₃ effected similar depolarization. CCK₈-evoked depolarization imitated the depolarization produced either by colon distension or by nerve stimulation. Upon repeated administration of CCK₈, the response of the cells to the peptide underwent tachyphylaxis. In addition, CCK₈ desensitized the depolarization evoked by stimulation in 50% of the cells. Furthermore, in an equal percentage of neurons, CCK₈ depressed responses of the colon distension-induced depolarization. The CCK₈ has both pre- and postsynaptic sites of action is supported by lowering Ca²⁺ and administering TTX (3 μM), which caused no effect and depressed 30% of CCK-induced depolarization respectively. Spantide (SP antagonist) blocked the response to SP, but not to CCK₈, in 5 out of 6 neurons, indicating separate receptor sites for SP and CCK₈. Moveover, completely desensitizing the cell response to SP or VIP did not cross desensitize its response to CCK₈ as observed in 6 neurons. In the rabbit IMG, the physiological significance of CCK₈ excitation is unknown, since colon distension did not elicit any depolarization. These results support the hypothesis that CCK₈ or a related peptide is a neurotransmitter mediating reflex activity between the colon and the IMG in guinea pig.
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Djabella, Karima. "MODELISATION DE L'ACTIVITE ELECTRIQUE DU COEUR ET DE SA REGULATION PAR LE SYSTEME NERVEUX AUTONOME." Phd thesis, Université Paris Sud - Paris XI, 2008. http://tel.archives-ouvertes.fr/tel-00335673.

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Nous avons développé un modèle de l'activité électrique cardiaque cellulaire dont la structure est moins complexe, sans pour autant affecter les caractéristiques essentielles (potentiel d'action, principaux courants ioniques, courbe de restitution). En outre, nous avons utilisé la même structure de modèle pour représenter l'activité électrique des divers types de cellules cardiaques. Cela permettra de déterminer des régions cardiaques de façon paramétrique et simplifiera l'identification des paramètres dans les modèles numériques de cœur. Par ailleurs, l'analyse de bifurcation nous a permis de retrouver l'origine du régime oscillatoire dans le cas pacemaker, et d'introduire un courant de fuite de calcium qui joue le rôle d'une entrée de commande pour le système nerveux autonome qui lui permet de modifier la fréquence cardiaque. D'autre part, il n'est plus possible de simplifier plus le modèle à l'aide de la méthode des perturbations singulières car ce n'est plus un système de Tikhonov. Le modèle permet une mise en œuvre en boucle fermée tenant compte du contrôle du système cardiovasculaire par l'arc baroréflexe et un couplage excitation-contraction tenant compte de l'effet de la fréquence sur la contractilité. <br />Après avoir démontré la non-existence de solutions périodiques dans le modèle réduit à deux courants ioniques de Mitchell-Schaeffer, nous avons introduit une variante de ce dernier et ainsi étendu ses propriétés d'excitabilité. Le régime oscillatoire est obtenu, soit à travers une bifurcation de Hopf sous ou super critique, soit à travers une bifurcation nœud-col sur cercle invariant. Ce modèle réduit est utilisable dans des applications de traitement du signal ECG.
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N'GUYEN, JEAN-MICHEL. "Systeme nerveux autonome et memoire de la cellule b-pancreatique au glucose chez le rat." Paris 7, 1994. http://www.theses.fr/1994PA077342.

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Le fait que l'effet potentialisateur de l'hyperglycemie prolongee sur la secretion d'insuline s'observe in vivo mais pas in vitro suggere l'implication de facteurs extrapancreatiques dans la memoire de la cellule b au glucose in vivo. Nous avons etudie le role possible du systeme nerveux autonome. Chez les rats rendus prealablement hyperglycemiques par une perfusion (48h) du glucose, nous avons montre: 1) l'implication d'une augmentation du tonus parasympathique et d'une diminution du tonus sympathique d'une part par enregistrement de l'activite electrique spontanee et d'autre part par des tests de secretion d'insuline apres vagotomie ou en presence d'un agoniste adrenergique, l'oxymetazoline. 2) ces alterations d'activite du systeme nerveux autonome sont dues a des changements au niveau du systeme nerveux central et a des modifications de la sensibilite de la cellule b aux neuromediateurs du systeme nerveux autonome. 3) une augmentation du debit sanguin insulaire qui est liee en grande partie a l'hyperactivite du systeme parasympathique alors que la diminution du tonus sympathique ne semble pas jouer de role important. L'ensemble de ce travail fournit de nombreux arguments en faveur d'une participation du systeme nerveux autonome au phenomene de memoire au glucose de la cellule b in vivo et suggere l'existence d'une boucle de regulation peut etre en circuit ferme liant la glycemie, l'activite du systeme nerveux autonome et la secretion d'insuline
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BISMUTH, TIBI DOMINIQUE. "Infection a v. I. H. , surrenales et systeme nerveux autonome : exploration biologique chez 20 patients infectes." Nice, 1989. http://www.theses.fr/1989NICE6579.

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Books on the topic "Ganglions du systeme nerveux autonome"

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McLachlan, A. J. Autonomic Ganglia (Autonomic Nervous System). Informa Healthcare, 1995.

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Geoffrey, Burnstock, and Hoyle, Charles H. V., 1955-, eds. Autonomic neuroeffector mechanisms. Harwood Academic Publishers, 1992.

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Structure of the Autonomic Nervous System. Springer, 2011.

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Otto, Appenzeller, ed. The autonomic nervous system. Elsevier Science Publishers, 1999.

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Geoffrey, Burnstock, and Sillito A. M, eds. Nervous control of the eye. Harwood Academic, 2000.

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Book chapters on the topic "Ganglions du systeme nerveux autonome"

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Purves, Dale, David A. Johnson, and Richard I. Hume. "Regulation of Synaptic Connections in the Rabbit Ciliary Ganglion." In Ciba Foundation Symposium 83 - Development of the Autonomic Nervous System. John Wiley & Sons, Ltd., 2008. http://dx.doi.org/10.1002/9780470720653.ch12.

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Atkinson, Martin E. "The autonomic nervous system." In Anatomy for Dental Students. Oxford University Press, 2013. http://dx.doi.org/10.1093/oso/9780199234462.003.0025.

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A large part of the nervous system is dedicated to the control of the internal viscera and their functions. Much of the activity of these organs is controlled reflexly at the brainstem level, e.g. the cardiovascular and respiratory centres (the vital centres) in the reticular formation of the medulla controlling cardiac and respiratory activity. There are also centres in the cerebrum, notably the hypothalamus in the diencephalon. Somatic and visceral functions are closely integrated at these higher levels; think of the effect that emotional factors or somatic stimulation can have on heart rate, blood pressure, and gastrointestinal activity when we are nervous or are in pain. The nerves involved in these activities are described as visceral sensory or visceral motor nerves because they control visceral function; this distinguishes them from somatic sensory nerves from peripheral receptors and somatic motor nerves controlling voluntary function. Visceral motor neurons innervate smooth muscle and secretory cells of the gastrointestinal and respiratory systems, the smooth and cardiac muscle of the cardiovascular system, the sweat glands and arrector pili muscles of the skin, and the muscles of the ciliary body and iris of the eyeball. In many cases, there is a dual supply from the sympathetic and parasympathetic divisions of the autonomic nervous system. In both divisions of the autonomic nervous system, there is a sequence of two neurons between the CNS and the effector organ which synapse in peripheral autonomic ganglia. The neurons from the CNS to the synapse in the ganglion are the preganglionic neurons and those from the ganglia to the effector organs are the postganglionic neurons. The enteric plexus is a third set of neurons interposed between the post-ganglionic neurons and the effector cells in the gastrointestinal tract. Figure 17.1 compares the general arrangement of the sympathetic and parasympathetic nervous system. The cell bodies of sympathetic visceral preganglionic motor neurons are located in the intermediolateral horns of the thoracic and upper lumbar segments of the spinal cord while those of the parasympathetic visceral preganglionic (secretomotor) neurons are in the nuclei of four of the cranial nerves and the sacral segments of the spinal cord.
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Cheshire, William P. "Autonomic Physiology." In Clinical Neurophysiology. Oxford University Press, 2009. http://dx.doi.org/10.1093/med/9780195385113.003.0035.

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The autonomic nervous system consists of three divisions: the sympathetic (thoracolumbar), parasympathetic (craniosacral), and enteric nervous systems. The sympathetic and parasympathetic autonomic outflows involve a two-neuron pathway with a synapse in an autonomic ganglion. Preganglionic sympathetic neurons are organized into various functional units that control specific targets and include skin vasomotor, muscle vasomotor, visceromotor, pilomotor, and sudomotor units. Microneurographic techniques allow recording of postganglionic sympathetic nerve activity in humans. Skin sympathetic activity is a mixture of sudomotor and vasoconstrictor impulses and is regulated mainly by environmental temperature and emotional influences. Muscle sympathetic activity is composed of vasoconstrictor impulses that are strongly modulated by arterial baroreceptors. Heart rate is controlled by vagal parasympathetic and thoracic sympathetic inputs. Vagal influence on the heart rate is strongly modulated by respiration; it is more marked during expiration and is absent during inspiration. This is the basis for the so-called respiratory sinus arrhythmia, which is an important index of vagal innervation of the heart. Power spectral analysis of heart rate fluctuations allows noninvasive assessment of beat-to-beat modulation of neuronal activity affecting the heart. Arterial baroreflex, cardiopulmonary reflexes, venoarteriolar reflex, and ergoreflexes control sympathetic and parasympathetic influences on cardiovascular effectors. The main regulatory mechanism that prevents orthostatic hypotension is reflex arterial vasoconstriction in the splanchnic, renal, and muscular beds triggered by a decrease in transmural pressure at the level of carotid sinus baroreceptors.
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Miller, Sarah, Laurence Watkins, and Manjit S. Matharu. "Trigeminal autonomic cephalalgias I: peripheral neuromodulation (occipital nerve and sphenopalatine ganglion stimulation)." In Surgery of the Autonomic Nervous System. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199686407.003.0011.

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