scholarly journals Letter by Aksu et al Regarding Article, “Relation of Fractionated Atrial Potentials With the Vagal Innervation Evaluated by Extracardiac Vagal Stimulation During Cardioneuroablation”

2020 ◽  
Vol 13 (8) ◽  
Author(s):  
Tolga Aksu ◽  
Tumer Erdem Guler ◽  
Rakesh Gopinathannair
Keyword(s):  
Vagal Stimulation ◽  
Vagal Innervation

Efferent vagal innervation of canine ventricle

1985 ◽  
Vol 248 (1) ◽  
pp. H89-H97 ◽  
Author(s):  
N. Takahashi ◽  
M. J. Barber ◽  
D. P. Zipes
Keyword(s):  
Coronary Artery ◽  
Vagal Stimulation ◽  
Left Ventricular ◽  
Constant Infusion ◽  
Epicardial Surface ◽  
Before And After ◽  
Vagal Innervation ◽  
The Subject ◽  
Infusion Of Norepinephrine ◽  
The Right

The route efferent vagal fibers travel to reach the left ventricle is not clear and was the subject of this investigation. We measured left ventricular and septal effective refractory period (ERP) changes during vagal stimulation and a constant infusion of norepinephrine, before and after phenol was applied at selected sites of the heart to interrupt efferent vagal fibers that may be traveling in that area. Phenol applied to the atrioventricular (AV) groove between the origin of the right coronary artery anteriorly to the posterior descending branch of the circumflex coronary artery completely eliminated vagal-induced prolongation of ERP in the anterior and posterior left ventricular free wall and reduced, but did not eliminate, ERP prolongation in the septum. A large (3-cm radius) epicardial circle of phenol prevented vagal-induced ERP prolongation within the circle in all dogs, while a small (1-cm radius) epicardial circle of phenol failed to prevent vagal-induced ERP changes within the circle in any dog. An intermediate (2-cm radius) circle eliminated vagal effects on ERP in 13 of 18 dogs. Arcs of phenol, to duplicate the upper portion of the circle, applied sequentially from apex to base eliminated efferent vagal effects only when painted near or at the AV groove. We conclude that the majority of efferent vagal fibers enroute to innervate the anterior and posterior left ventricular epicardium cross the AV groove within 0.25-0.5 mm (depth of phenol destruction) of the epicardial surface.(ABSTRACT TRUNCATED AT 250 WORDS)

Compensatory recovery of parasympathetic control of heart rate after unilateral vagotomy in rabbits

1992 ◽  
Vol 262 (4) ◽  
pp. H1122-H1127 ◽  
Author(s):  
D. D. Lund ◽  
G. A. Davey ◽  
A. R. Subieta ◽  
B. J. Pardini
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Nerve Stimulation ◽  
Vagal Stimulation ◽  
Acetylcholinesterase Inhibition ◽  
Baroreflex Control ◽  
Recovery Mechanism ◽  
Vagal Innervation ◽  
Increased Sensitivity ◽  
Parasympathetic Control

Compensatory recovery by the intact vagal innervation after unilateral vagotomy was investigated by measuring parasympathetic-mediated control of heart rate in beta-adrenergic-blocked rabbits. Direct contralateral vagal nerve stimulation produced greater bradycardia in anesthetized rabbits with chronic vagotomy compared with acutely vagotomized controls. Vagal stimulation during acetylcholinesterase inhibition by physostigmine and direct neuroeffector stimulation by methacholine indicated that a change in metabolism of the neurotransmitter or an increased sensitivity of the tissue to acetylcholine were not responsible for augmentation of vagal responses. Baroreflex control of heart rate in response to an increase in arterial pressure was also tested in urethan-anesthetized rabbits. There was a significant reduction in the prolongation of the R-R interval during baroreflex activation acutely after midcervical vagotomy. These values were subsequently above control levels in rabbits 28 days after vagotomy. In conscious rabbits, the decrease in baroreflex control of heart rate progressively recovered to control levels within 6 days. These results suggest that the recovery mechanism after unilateral vagotomy may be related to peripheral and central compensatory changes in the intact contralateral vagus nerve.

Electrophysiological identification of vagally innervated enteric neurons in guinea pig stomach

1992 ◽  
Vol 263 (5) ◽  
pp. G709-G718 ◽  
Author(s):  
M. Schemann ◽  
D. Grundy
Keyword(s):  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Enteric Neurons ◽  
Command Neurons ◽  
Myenteric Neurons ◽  
Release Of Acetylcholine ◽  
Vagal Innervation ◽  
Guinea Pig Stomach ◽  
Stimulation Of

Myenteric "command neurons" are thought to be the interface between extrinsic and intrinsic controls of gut functions and are thought to be responsible for transmission of vagal impulses to enteric microcircuits. To identify, electrophysiologically, myenteric neurons responding to electrical stimulation of the vagus, we developed an in vitro preparation of the gastric myenteric plexus in which the vagal innervation was preserved. The majority of myenteric neurons [102 of 155 (66%)] received fast excitatory postsynaptic potentials (fEPSPs) after stimulation of the vagus. The proportion of neurons receiving vagal input was highest at the lesser curve (98%) and decreased gradually when recordings were made from neurons located toward the greater curve. Only a small proportion of neurons (4 of 85 cells) showed a slow EPSP after a burst of vagal stimulation. No postsynaptic inhibitory potentials were observed. There was no preferential vagal input to either gastric I, gastric II, or gastric III neurons. The fEPSPs were due to the release of acetylcholine acting postsynaptically on nicotinic receptors. The behavior of the fEPSPs suggests multiple vagal inputs to a majority of myenteric neurons. Our observations call into question the concept of enteric command neurons in favor of a divergent vagal input with widespread modulatory influences over gastric enteric neurotransmission.

Vagal control of central and peripheral pulmonary resistance in developing piglets

1991 ◽  
Vol 70 (4) ◽  
pp. 1617-1626 ◽  
Author(s):  
J. J. Perez Fontan ◽  
A. O. Ray
Keyword(s):  
Vagal Stimulation ◽  
Muscle Tone ◽  
Positive Pressure ◽  
Large Contribution ◽  
Postnatal Maturation ◽  
Peripheral Airways ◽  
Vagal Control ◽  
Vagal Innervation ◽  
Lung Periphery ◽  
Alpha Chloralose

To study the postnatal maturation of vagal control of airway muscle tone, we determined the effects of vagotomy and supramaximal vagal stimulation on the resistance of the respiratory system in eight newborn and seven 6-wk-old piglets. Because the lung periphery has distinctive responses to cholinergic agonists and a lower density of vagal fibers and cholinergic receptors than the central airways, we partitioned the respiratory resistance of the piglets between central airways (Rc) and peripheral airways and lung tissue (Rp) with bronchial catheters inserted in a retrograde manner. The piglets were anesthetized with alpha-chloralose and ventilated with positive airway pressure. Vagotomy did not change Rc or Rp in either the newborn or the 6-wk-old piglets. Vagal stimulation, on the other hand, increased both Rc (median increase 53% in the newborn and 72% in the 6-wk-old piglets) and Rp (54 and 42%, respectively). At all states of vagal tone, Rp increased as the lungs were inflated, suggesting a large contribution of tissue viscoelasticity to this resistance. Our results demonstrate that vagal bronchomotor tone is absent during mechanical ventilation with positive pressure in the developing piglet. However, vagal innervation of both central airways and tissue contractile elements is functionally competent at the time of birth in this species.

scholarly journals Some Aspects of the Physiology and Anatomy of the Cardiovascular System of the Ferret, Mustela Putorius Furo

1979 ◽  
Vol 13 (3) ◽  
pp. 215-220 ◽  
Author(s):  
P. L. R. Andrews ◽  
A. J. Bower ◽  
O. Illman
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Vagal Stimulation ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Resting Heart Rate ◽  
Mustela Putorius ◽  
Arterial Blood ◽  
Great Vessels ◽  
Vagal Innervation

Summary The resting heart rate was monitored in SO urethane-anaesthetized (387 ± 54 beats/min) and 4 conscious (341 ± 39 beats/min) ferrets. The arterial blood pressure in the anaesthetized animals was 140/110 ± 35/31 mmHg. The circulatory responses to vagal stimulation, carotid artery occlusion and a variety of humoral agents were examined. The vagal innervation of the heart and of the distribution of the great vessels are described.

scholarly journals Effect of Electrical Stimulation of the Vagus Nerves on Bile Secretion in Anaesthetized Sheep

1976 ◽  
Vol 29 (4) ◽  
pp. 351 ◽  
Author(s):  
MichaeI Pass ◽  
Trevor Heath
Keyword(s):  
Electrical Stimulation ◽  
Bile Salt ◽  
Maximum Rate ◽  
Vagal Stimulation ◽  
Bile Secretion ◽  
Vagus Nerves ◽  
Bile Formation ◽  
Vagal Innervation ◽  
Bicarbonate Output ◽  
Stimulation Of

Bile was collected before and during electrical stimulation of the vagus nerves in acute experiments on sheep with ligated cystic ducts. Most stimuli caused no change in: bile formation, but a 10-V, 10-Hz stimulus caused a slight increase in bicarbonate output. Neither the response to infused secretin nor the maximum rate of bile salt transpoit by liver cells changed during vagal stimulation; It was concluded that the vagal innervation of the liver is not likely to playa major role in the regulation of bile formation in sheep.

scholarly journals Relation of Fractionated Atrial Potentials With the Vagal Innervation Evaluated by Extracardiac Vagal Stimulation During Cardioneuroablation

2020 ◽  
Vol 13 (4) ◽  
Author(s):  
Enrique I. Pachon-M ◽  
Jose Carlos Pachon-Mateos ◽  
Christian Higuti ◽  
Tomas G. Santillana-P ◽  
Tasso Lobo ◽  
...  
Keyword(s):  
Vagal Stimulation ◽  
Vagal Innervation

Effect of thoracic vagotomy and vagal stimulation on esophageal function.

1978 ◽  
Vol 234 (4) ◽  
pp. E359 ◽  
Author(s):  
J J Kravitz ◽  
W J Snape ◽  
S Cohen
Keyword(s):  
Electrical Stimulation ◽  
Vagal Stimulation ◽  
Esophageal Function ◽  
Primary Peristalsis ◽  
Vagal Innervation ◽  
Relaxation Responses ◽  
Secondary Peristalsis ◽  
Thoracic Vagotomy ◽  
Upper Thoracic ◽  
Stimulation Of

The purpose of this study was to determine the effect of thoracic vagotomy and thoracic vagal stimulation upon esophageal peristalsis and lower esophageal sphincter (LES) function in the opossum. The thoracic portion of the vagus nerve was sectioned in the upper or lower thorax. Bilateral, but not unilateral, thoracic vagotomy above the level of the heart abolished peristalsis and LES relaxation in response to swallowing or cervical vagal electrical stimulation. Thoracic vagotomy at the level of the ventricle or below did not alter either peristalsis or LES relaxation during swallowing or cervical vagal stimulation. Secondary peristalsis and its associated LES relaxation was unaltered by thoracic vagotomy at any level. Electrical stimulation of the distal end of the upper thoracic vagus elicited both peristalsis and LES relaxation. Electrical stimulation of the distal end of the lower thoracic vagus elicited both peristalsis and LES relaxation. Electrical stimulation of the distal end of the lower thoracic vagus, as well as stimulation of the vagal branches to the terminal esophagus, gave only LES relaxation. These studies suggest that: a) the major extrinsic vagal innervation mediating primary peristalsis terminates in the upper portion of the esophagus, whereas the vagal innervation mediating LES relaxation responses are present throughout the length of the esophagus; and b) secondary peristalsis and its associated LES relaxation occurs independent of extrinsic vagal innervation.

Topography of efferent vagal innervation of the rat gastrointestinal tract

1991 ◽  
Vol 260 (1) ◽  
pp. R200-R207 ◽  
Author(s):  
H. R. Berthoud ◽  
N. R. Carlson ◽  
T. L. Powley
Keyword(s):  
Vagal Stimulation ◽  
The Other ◽  
Motor Nucleus ◽  
Anterograde Tracing ◽  
Entire Colon ◽  
Dorsal Motor Nucleus ◽  
Carbocyanine Dye ◽  
Vagal Innervation ◽  
Hepatic Branch ◽  
Entire Stomach

The gastrointestinal territories innervated by the gastric, celiac, and hepatic abdominal vagi were identified in rats with selective branch vagotomies by means of 1) anterograde tracing with the carbocyanine dye DiI injected into the dorsal motor nucleus and 2) measurement of cervical vagal stimulation-induced motility responses throughout the gut axis. Presence of DiI-labeled vagal terminals in the myenteric plexus and evoked motility responses were well correlated across the sampled gastrointestinal (GI) sites. In animals with only the two gastric branches intact, the entire stomach and the most proximal duodenum showed significant motility responses and were densely innervated, having DiI-labeled vagal terminals in almost every ganglion. The hepatic branch was found to primarily innervate the duodenum, with minor projections to the distal antral stomach and the intestines. The two celiac branches were found to almost exclusively innervate the jejunum, ileum, cecum and entire colon, and, together with the other vagal branches, the duodenum. Therefore, while there is some degree of specific innervation by the abdominal vagal branches of the oral-to-anal gut axis, which could be called "viscerotopic," the considerably overlapping innervation of the duodenum does not satisfy a viscerotopy criterion and needs further functional analysis.

GRP nerves in pig antrum: role of GRP in vagal control of gastrin secretion

1987 ◽  
Vol 253 (5) ◽  
pp. G643-G649 ◽  
Author(s):  
J. J. Holst ◽  
S. Knuhtsen ◽  
C. Orskov ◽  
T. Skak-Nielsen ◽  
S. S. Poulsen ◽  
...  
Keyword(s):  
Substance P ◽  
Vagal Stimulation ◽  
Nerve Fibers ◽  
Gastrin Cells ◽  
Gastrin Secretion ◽  
Substance P Antagonist ◽  
Vagal Nerves ◽  
Vagal Innervation ◽  
Dose Dependent

We extracted gastrin-releasing peptide (GRP) and its C-terminal decapeptide corresponding to 6.4 and 6.8 pmol/g from pig antrum mucosa. By immunohistochemistry GRP was localized to mucosal, submucosal, and myenteric nerve fibers. A few nerve cell bodies were also identified. Using isolated perfused pig antrum with intact vagal innervation, we found concomitant, atropine-resistant release of GRP and gastrin during electrical stimulation of the vagal nerves. Intra-arterial GRP at 10(-11)-10(-10) mol/l caused up to fivefold, dose-dependent increases in gastrin secretion; higher doses were less effective and completely desensitized the gastrin cells for the lower doses. After desensitization, vagal stimulation no longer produced gastrin secretion. The substance P antagonist [D-Arg, D-Pro, D-Trp, Leu]-substance P, described as also antagonizing the actions of bombesin, decreased the gastrin response to GRP and abolished the effect of vagal stimulation. The available evidence strongly suggests that GRP nerves are responsible for the stimulatory vagal effects on gastrin secretion in the pig.

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