Role of the Vagus Nerve in the Antidysrhythmic Effect of Dexmedetomidine on Halothane/Epinephrine Dysrhythmias in Dogs

1995 ◽  
Vol 83 (5) ◽  
pp. 992-999 ◽  
Author(s):  
Takahiko Kamibayashi ◽  
Yukio Hayashi ◽  
Tadanori Mammoto ◽  
Atsushi Yamatodani ◽  
Koji Sumikawa ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Vagus Nerve ◽  
Neural Activity ◽  
Vagal Stimulation ◽  
Adrenergic Agonist ◽  
The Central Nervous System ◽  
Stimulation Of

Abstract Background Dexmedetomidine, an alpha2-adrenergic agonist, can prevent the genesis of halothane/epinephrine dysrhythmias through the central nervous system. Because stimulation of alpha2adrenoceptors in the central nervous system enhances vagal neural activity and vagal stimulation is known to inhibit digitalis-induced dysrhythmias, dexmedetomidine may exert the antidysrhythmic property through vagal stimulation. To address this hypothesis, the effect of dexmedetomidine in vagotomized dogs was examined and compared with that in intact dogs. In addition, the effect of vagotomy on the antidysrhythmic action of doxazosin, an alpha1antagonist, was studied.

scholarly journals Role of Catecholamine in Pressor Responses to Stimulation of the Central Nervous System

1963 ◽  
Vol 4 (2) ◽  
pp. 118-130 ◽  
Author(s):  
Hideo UEDA ◽  
Akiyuki YAMADA ◽  
Hitoshi GOTO ◽  
Iwao ITO ◽  
Yutaka TAKABATAKE ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Pressor Responses ◽  
The Central Nervous System ◽  
Stimulation Of

scholarly journals Role of L-glutamate in aggression

2016 ◽  
Vol 72 (12) ◽  
pp. 740-744
Author(s):  
Bogdan Feliks Kania ◽  
Danuta Wrońska
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Steroid Receptors ◽  
Cation Channels ◽  
Metabotropic Receptor ◽  
Ionotropic Receptors ◽  
The Central Nervous System ◽  
G Protein Coupled ◽  
Stimulation Of

L-glutamate is one of major excitatory transmitters (along with aspartic, kainate acids and glycine) in the central nervous system and/or the peripheral nervous system. It mediates interaction through the stimulation of various ionotropic receptors families (ligand gated cation channels) and metabotropic receptor families (G-protein coupled). In this review, we describe the molecular composition of these glutamatergic receptors and discuss their neuropharmacology, particularly with respect to their roles in animal social behaviors and, particularly, in aggression. It is also known, that during aggression different interactions occur in the nervous system among glutamate, serotonin, vasopressin, oxytocin, dopamine, GABA and steroid receptors.

TRH-induced vagal stimulation of duodenal HCO-3 mediated by VIP and muscarinic pathways

1989 ◽  
Vol 257 (5) ◽  
pp. G677-G682 ◽  
Author(s):  
H. J. Lenz ◽  
W. W. Vale ◽  
J. E. Rivier
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Intravenous Administration ◽  
Vagal Stimulation ◽  
Bicarbonate Secretion ◽  
Endogenous Opiates ◽  
Duodenal Bicarbonate Secretion ◽  
The Central Nervous System ◽  
Freely Moving ◽  
Stimulation Of

The central nervous system effects of thyrotropin-releasing hormone (TRH) on proximal duodenal bicarbonate secretion were studied in freely moving rats. Cerebroventricular administration of TRH (0.5-5.0 nmol) significantly stimulated basal duodenal bicarbonate secretion, whereas intravenous administration of TRH did not. Ganglionic blockade with chlorisondamine and truncal vagotomy abolished TRH-induced bicarbonate secretion, whereas atropine significantly attenuated the response. The vasoactive intestinal peptide (VIP) receptor antagonist, (4Cl-D-Phe6, Leu17) VIP given intravenously completely prevented the stimulatory effect of central TRH on duodenal bicarbonate secretion. In contrast, hypophysectomy, adrenalectomy, opiate and noradrenergic blockade, or indomethacin did not affect the TRH-induced bicarbonate response. Intravenous administration of VIP and carbachol significantly stimulated bicarbonate outputs, and these responses were blocked by the VIP antagonist and atropine, respectively. These results indicate that TRH may serve as a central nervous system mediator that stimulates duodenal bicarbonate secretion in rats by increasing vagal outflow. Vagal stimulation induced by TRH increases duodenal bicarbonate secretion by the release of VIP and, in part, by activation of a muscarinic pathway but not by pituitary, adrenal, and noradrenergic pathways or endogenous opiates and prostaglandins. The actions of peripheral VIP and carbachol appear to be mediated by specific VIP and muscarinic receptors, respectively.

scholarly journals Role of GABA-A and GABA-B receptors of the brain in the hypothalamo-pituitary-testicular regulation by the negative feedback mechanism

1995 ◽  
Vol 41 (4) ◽  
pp. 36-38
Author(s):  
Ye. V. V. Naumenko ◽  
A. V. Amikishiyeva ◽  
L. I. Serova
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Negative Feedback ◽  
Feedback Mechanism ◽  
Gaba A ◽  
Negative Feedback Mechanism ◽  
The Central Nervous System ◽  
The Brain ◽  
Stimulation Of

The role of gamma-aminobutyric acid (GABA) of the brain and its receptors in the hypothalamo-pituitary-testicular (HPT) regulation by the negative feedback mechanism was for the first time studied in sham-operated and unilaterally castrated adult Wister rats. Increased level of GABA in the central nervous system following an injection of GABA transaminase inhibitor, aminoacetic acid, into the lateral ventricle of the brain was associated with activation of a compensatory increase of testosterone level in the blood, caused by unilateral castration. GABA effect is mediated through the receptors. Muscimol stimulation of GABA-A receptors of the central nervous system activated and their blocking with bicucullin inhibited a compensatory increase of testosterone level in the blood caused by hemicastration. Baclofen stimulation of cerebral GABA-B receptors was associated with an inhibition and their saclofen blocking with stimulation of the level of male sex steroid hormone in the blood following unilateral castration. A conclusion is made about participation of GABAergic mechanisms of the brain in the regulation of HPT function via the negative feedback mechanism

The contribution of afferent signals from the liver to metabolic regulation during exercise

2002 ◽  
Vol 80 (11) ◽  
pp. 1035-1044 ◽  
Author(s):  
Jean-Marc Lavoie
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Blood Glucose ◽  
Food Intake ◽  
Vagus Nerve ◽  
Metabolic Regulation ◽  
Vagal Activity ◽  
The Central Nervous System ◽  
Response To Exercise

The crucial role of the liver as the only organ to produce glucose used by skeletal muscle during exercise is well known. Since hepatic glucose production is central to blood glucose homeostasis during exercise, it has been postulated that the liver may inform the central nervous system and other organs of its diminishing capacity to produce glucose from glycogen, before blood glucose falls. The sensory role of the liver during exercise would be similar to its role in the control of food intake. As a consequence, the experimental approaches used to test the hypothesis that afferent signals from the liver contribute to metabolic regulation during exercise are inspired by those used to test the same hypothesis in the regulation of food intake. In the present review, two questions are addressed. The existing evidence for the liver's sensory influence on metabolic adjustments to exercise is first reviewed; the nature of the initiating stimuli for the afferent contribution of the liver to physical exercise is discussed thereafter. The hypothetical construct upon which rests the contribution of the liver's afferent signals to metabolic regulation during exercise is that a decrease in liver glycogen or a related metabolic intermediate is sensed by the liver, and the signal is transduced to the central nervous system, most likely through the afferent activity of the hepatic vagus nerve, where it contributes to the orchestration of the metabolic and hormonal responses to exercise. Support in favour of this construct comes mainly from the demonstration that sectioning of the hepatic vagus nerve attenuates the normal hormonal response to exercise. It seems that the liver–glucagon axis is particularly responsive to this reflex activation. In other respects, the hepatic mechanism responsible for linking the metabolic activity in the liver to an afferent signal capable of regulating the metabolic response to exercise remains speculative. Substrates or derivatives of substrate oxidation, energy-related compounds (ATP and Pi), or changes in cell volume may all be related to changes in transmembrane potential in the liver cell, which according to the "potentiostatic" theory would determine the afferent vagal activity. Key words: hepatic vagotomy, insulin, glucagon, portal infusion, metabolic regulation.

Role of a nurse in the rehabilitation of children using ReviMotion hardware and software complex

2020 ◽  
pp. 49-56
Author(s):  
T. Shirshova
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
School Age Children ◽  
Equipment Management ◽  
School Age ◽  
Rehabilitation Process ◽  
Software Complex ◽  
Trained Personnel ◽  
The Central Nervous System

Disorders of the musculoskeletal system in school-age children occupy 1-2 places in the structure of functional abnormalities. Cognitive impairment without organic damage to the central nervous system is detected in 30-56% of healthy school children. Along with the increase in the incidence rate, the demand for rehabilitation systems, which allow patients to return to normal life as soon as possible and maintain the motivation for the rehabilitation process, is also growing. Adaptation of rehabilitation techniques, ease of equipment management, availability of specially trained personnel and availability of technical support for complexes becomes important.

The Role of Neuropeptide Y and Peptide YY in the Development of Obesity via Gut-brain Axis

2019 ◽  
Vol 20 (7) ◽  
pp. 750-758 ◽  
Author(s):  
Yi Wu ◽  
Hengxun He ◽  
Zhibin Cheng ◽  
Yueyu Bai ◽  
Xi Ma
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Neuropeptide Y ◽  
Metabolic Diseases ◽  
Peptide Yy ◽  
Vital Role ◽  
Gut Peptides ◽  
Nonalcoholic Fatty Liver ◽  
The Central Nervous System

Obesity is one of the main challenges of public health in the 21st century. Obesity can induce a series of chronic metabolic diseases, such as diabetes, dyslipidemia, hypertension and nonalcoholic fatty liver, which seriously affect human health. Gut-brain axis, the two-direction pathway formed between enteric nervous system and central nervous system, plays a vital role in the occurrence and development of obesity. Gastrointestinal signals are projected through the gut-brain axis to nervous system, and respond to various gastrointestinal stimulation. The central nervous system regulates visceral activity through the gut-brain axis. Brain-gut peptides have important regulatory roles in the gut-brain axis. The brain-gut peptides of the gastrointestinal system and the nervous system regulate the gastrointestinal movement, feeling, secretion, absorption and other complex functions through endocrine, neurosecretion and paracrine to secrete peptides. Both neuropeptide Y and peptide YY belong to the pancreatic polypeptide family and are important brain-gut peptides. Neuropeptide Y and peptide YY have functions that are closely related to appetite regulation and obesity formation. This review describes the role of the gutbrain axis in regulating appetite and maintaining energy balance, and the functions of brain-gut peptides neuropeptide Y and peptide YY in obesity. The relationship between NPY and PYY and the interaction between the NPY-PYY signaling with the gut microbiota are also described in this review.

Sign in / Sign up

Export Citation Format

Share Document