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.

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)

Functional anatomy of the vagal innervation of the cervical trachea of the dog

2000 ◽  
Vol 89 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Robert L. Coon ◽  
Patrick J. Mueller ◽  
Philip S. Clifford
Keyword(s):  
Smooth Muscle ◽  
Vagus Nerve ◽  
Neural Control ◽  
Muscle Tone ◽  
Cuff Pressure ◽  
Vagal Innervation ◽  
Cervical Trachea ◽  
The Right ◽  
Left Vagus ◽  
Stimulation Of

The canine cervical trachea has been used for numerous studies regarding the neural control of tracheal smooth muscle. The purpose of the present study was to determine whether there is lateral dominance by either the left or right vagal innervation of the canine cervical trachea. In anesthetized dogs, pressure in the cuff of the endotracheal tube was used as an index of smooth muscle tone in the trachea. After establishment of tracheal tone, as indicated by increased cuff pressure, either the right or left vagus nerve was sectioned followed by section of the contralateral vagus. Sectioning the right vagus first resulted in total loss of tone in the cervical trachea, whereas sectioning the left vagus first produced either a partial or no decrease in tracheal tone. After bilateral section of the vagi, cuff pressure was recorded during electrical stimulation of the rostral end of the right or left vagus. At the maximum current strength used, stimulation of the left vagus produced tracheal constriction that averaged 28.5% of the response to stimulation of the right vagus (9.0 ± 1.8 and 31.6 ± 2.5 mmHg, respectively). In conclusion, the musculature of cervical trachea in the dog appears to be predominantly controlled by vagal efferents in the right vagus nerve.

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.

Interaction of lung volume and chemical drive on respiratory muscle EMG and respiratory timing

1977 ◽  
Vol 42 (2) ◽  
pp. 287-295 ◽  
Author(s):  
S. G. Kelsen ◽  
M. D. Altose ◽  
N. S. Cherniack
Keyword(s):  
Electrical Activity ◽  
Lung Volume ◽  
Respiratory Muscle ◽  
Vagal Stimulation ◽  
Abdominal Muscle ◽  
Positive Pressure ◽  
Airway Occlusion ◽  
Continuous Positive Pressure ◽  
Spontaneously Breathing

The effect of increased FRC on the change in respiratory muscle electrical activity (EMG) and the duration of inspiration (Ti) and expiration (Te) produced by increases in chemical drive (i.e., progressive hypercapnia and isocapnic hypoxia) was assessed in 15 anesthetized, spontaneously breathing dogs. FRC was raised by applying continuous positive pressure (4 and 8 cmH2O) to the airway. Progressive hypercapnia and hypoxia were produced by rebreathing techniques. At any PCO2 or PO2, increases in FRC decreased diaphragm EMG (D); increased abdominal muscle EMG (AB); and prolonged Te without affecting Ti. The effect of increased FRC on D, AB, and Te diminished as PCO2 increased or PO2 decreased. The effect of sustained increases in lung volume in the absence of phasic changes was assessed by performing airway occlusion for a single inspiration during rebreathing at both control and increased FRC. The effects of increases in FRC were present during airway occlusion but were eliminated by vagotomy. We conclude, therefore, that tonic vagal stimulation produced by increases in FRC modified the change in respiratory muscle electrical activity and timing produced by increasing chemical drive.

Absence of nonadrenergic noncholinergic relaxation in the cat cervical trachea

1988 ◽  
Vol 65 (6) ◽  
pp. 2524-2530 ◽  
Author(s):  
H. Don ◽  
D. G. Baker ◽  
C. A. Richardson
Keyword(s):  
Smooth Muscle ◽  
Vagal Stimulation ◽  
Muscle Tone ◽  
Dynamic Compliance ◽  
Tracheal Mucosa ◽  
In Vivo Experiments ◽  
Lower Airways ◽  
Cervical Trachea

Published in vivo experiments have not supported in vitro reports of the presence of nonadrenergic noncholinergic (NANC) inhibitory pathways in the cat trachea. We therefore examined these pathways, measuring tension in an innervated tracheal segment, flow resistance in more distal airways, and dynamic compliance, in 10 anesthetized mechanically ventilated cats. Initially, cervical vagal stimulation evoked contraction followed by relaxation of smooth muscle of trachea and lower airways; sympathetic stimulation evoked relaxation only. After muscarinic blockade and restoration of smooth muscle tone with 5-hydroxytryptamine (5-HT) applied topically to the tracheal mucosa, vagal stimulation did not affect tracheal segment tension, whereas sympathetic-evoked relaxation was preserved. Similar results were found when tone was restored with intravenous 5-HT, with vagal stimulation also decreasing resistance and increasing compliance. We conclude that NANC pathways are present in lower airways but not in the cervical trachea of the cat. We hypothesize that parasympathetic constriction of cat airway smooth muscle can occur without simultaneous NANC activation, whereas NANC activity occurs only in tandem with parasympathetic stimulation.

Vagal neuroeffector mechanisms affecting transpulmonary pressure in the intact rat

1995 ◽  
Vol 79 (4) ◽  
pp. 1233-1241 ◽  
Author(s):  
J. R. Haselton ◽  
A. Y. Reynolds ◽  
H. D. Schultz
Keyword(s):  
Smooth Muscle ◽  
Untreated Control ◽  
Vagal Stimulation ◽  
Muscle Tone ◽  
Transpulmonary Pressure ◽  
Bilateral Stimulation ◽  
Vagus Nerves ◽  
Prostaglandin F2 Alpha ◽  
Combined Administration ◽  
Stimulation Of

Experiments were conducted with chloralose-urethan anesthetized rats to assess the effects of 1) bilateral stimulation of the cervical vagus nerves and 2) parasympathomimetic and sympathomimetic agents. Transpulmonary pressure (Ptp) was used as an index of airway smooth muscle tone, and peak inspiratory Ptp (Ptppeak) values were used for a comparison of responses. In untreated animals, vagal stimulation elicited an increase in Ptppeak of 155%. Cooling of the vagus nerves to 15 degrees C abolished the response of Ptppeak to vagal stimulation. Although isoproterenol (1–10 micrograms/kg i.v.) did not alter resting Ptppeak, it did prevent vagal stimulation from evoking an increase in Ptppeak. Nadolol (1.5 mg/kg i.v.) augmented the increase in Ptppeak elicited by vagal stimulation. Vagal stimulation did not evoke any change in Ptppeak after the administration of both nadolol and atropine or after combined administration of nadolol, atropine, and either serotonin aerosol or prostaglandin F2 alpha. In rats pretreated with capsaicin 1 wk before the experiment, vagal stimulation evoked an increase in Ptppeak that was not statistically different from that of untreated control animals. Therefore, nonadrenergic noncholinergic systems did not appear to play an independent role in the response of the airways to the activation of the vagus nerves.

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.

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.

Role of endothelium-derived relaxing factor in parasympathetic coronary vasodilation

1992 ◽  
Vol 262 (5) ◽  
pp. H1579-H1584 ◽  
Author(s):  
T. P. Broten ◽  
J. K. Miyashiro ◽  
S. Moncada ◽  
E. O. Feigl
Keyword(s):  
Vagal Stimulation ◽  
Specific Inhibitor ◽  
Coronary Vasodilation ◽  
Relaxing Factor ◽  
Inhibit Prostaglandin Synthesis ◽  
Constant Rate ◽  
Anesthetized Dogs ◽  
Endothelium Derived Relaxing Factor ◽  
Alpha Chloralose

Vasodilation following the infusion of acetylcholine is due to the release of endothelium-derived relaxing factor (EDRF). However, the role of EDRF in neurogenic coronary vasodilation, when acetylcholine is released outside the vessel at the adventitial-medial junction, has not been established. The action of EDRF in parasympathetic coronary vasodilation was tested in the present study using a specific inhibitor of EDRF synthesis, nitro-L-arginine methyl ester (L-NAME). Experiments were conducted on closed-chest, alpha-chloralose-anesthetized dogs with the heart paced at a constant rate. Phentolamine and propranolol were administered to block alpha- and beta-adrenergic receptors, and ibuprofen was given to inhibit prostaglandin synthesis. Intracoronary infusion of L-NAME decreased the coronary vasodilation in response to intracoronary acetylcholine or vagal stimulation. The coronary response to the endothelium-independent vasodilator nitroglycerin was unaffected by L-NAME. These data demonstrate that L-NAME specifically inhibits coronary vasodilation caused by acetylcholine and vagal stimulation, indicating that parasympathetic coronary vasodilation is dependent on EDRF.

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.

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