Interaction of serotonin with vagal- and ACh-induced bronchoconstriction in canine lungs

1982 ◽  
Vol 52 (4) ◽  
pp. 964-966 ◽  
Author(s):  
J. R. Sheller ◽  
M. J. Holtzman ◽  
B. E. Skoogh ◽  
J. A. Nadel
Keyword(s):  
Electrical Stimulation ◽  
Nerve Terminal ◽  
Vagal Stimulation ◽  
Vagus Nerves ◽  
Parasympathetic Ganglia ◽  
Anesthetized Dogs ◽  
Postganglionic Nerve ◽  
Stimulation Of

The bronchoconstrictor response to electrical stimulation of the peripheral ends of both cut cervical vagus nerves was potentiated by serotonin aerosols in 10 experiments in 7 anesthetized dogs. The bronchoconstrictor response to acetylcholine (ACh) aerosols was unchanged after serotonin. We conclude that serotonin acts at the level of the parasympathetic ganglia or the postganglionic nerve terminal to potentiate the bronchoconstrictor response to vagal stimulation.

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.

Vagal regulation of GRP, gastric somatostatin, and gastrin secretion in vitro

1985 ◽  
Vol 248 (4) ◽  
pp. E425-E431 ◽  
Author(s):  
S. Nishi ◽  
Y. Seino ◽  
J. Takemura ◽  
H. Ishida ◽  
M. Seno ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Nicotinic Receptors ◽  
Vagal Stimulation ◽  
Inhibitory Neuron ◽  
Atropine Sulfate ◽  
Vagus Nerves ◽  
Gastrin Secretion ◽  
Somatostatin Secretion ◽  
Stimulation Of

The effect of electrical stimulation of the vagus nerves on the release of immunoreactive gastrin-releasing peptide (GRP), gastrin, and somatostatin was investigated using the isolated perfused rat stomach. Electrical stimulation (10 Hz, 1 ms duration, 10 V) of the peripheral end of the subdiaphragmatic vagal trunks produced a significant increase in both GRP and gastrin but a decrease in somatostatin. The infusion of atropine sulfate at a concentration of 10(-5) M augmented GRP release and reversed the decrease in somatostatin release in response to vagal stimulation to an increase above basal levels. However, the gastrin response to vagal stimulation was not affected by atropine. The infusion of hexamethonium bromide at a concentration of 10(-4) M significantly suppressed GRP release but did not affect gastrin secretion in response to vagal stimulation. On the other hand, the somatostatin response to vagal stimulation was completely abolished by hexamethonium. These findings lead us to conclude that the intramural GRP neurons might play an important role in the regulation of gastrin as well as somatostatin secretion and that somatostatin secretion may be controlled not only by a cholinergic inhibitory neuron but also by a noncholinergic, e.g., peptidergic stimulatory neuron, both of which may be regulated through preganglionic vagal fibers via nicotinic receptors. In addition, because the infusion of 10(-7) M GRP suppressed the somatostatin secretion, we suggest that either GRP should be excluded from the list of candidates for the noncholinergic stimulatory neurotransmitter for somatostatin secretion or that there are different mechanisms of action for endogenous and exogenous GRP.

Bronchial reactivity: interaction between vagal stimulation and inhaled histamine

1977 ◽  
Vol 43 (4) ◽  
pp. 643-647 ◽  
Author(s):  
M. K. Benson ◽  
P. D. Graf
Keyword(s):  
Response Curve ◽  
Vagal Stimulation ◽  
Base Line ◽  
Bronchial Reactivity ◽  
Vagus Nerves ◽  
Airway Reactivity ◽  
Vagal Blockade ◽  
Anesthetized Dogs ◽  
Stimulation Of ◽  
Bronchomotor Tone

The interaction between the effects of vagal stimulation and inhaled histamine on the bronchi was studied in anesthetized dogs. Reactivity was assessed by measuring changes in bronchial caliber visualized with tantalum bronchograms. In seven vagotomized dogs the bronchoconstrictor response to a combination of electrical stimulation of the vagus nerves and inhaled histamine solution produced a mean reduction in airway diameter (Daw) of 2.21 mm which was significantly greater than the additive results of the two stimuli applied separately (mean decrease in Daw 0.29 +/- 0.91 mm). In three dogs the effect of vagal stimulation was to produce a shift in the dose-response curve to inhaled histamine. These results indicate that the effect of the base-line bronchomotor tone must be considered in the evaluation of the effect of vagal blockade on airway reactivity. An increase in the resting degree of bronchomotor tone may contribute to the hyperreactivity observed in patients with asthma.

Inhibition of respiratory reflexes by local anesthetic aerosols in dogs and rabbits

1975 ◽  
Vol 38 (6) ◽  
pp. 1045-1050 ◽  
Author(s):  
D. S. Dain ◽  
H. A. Boushey ◽  
W. M. Gold
Keyword(s):  
Electrical Stimulation ◽  
Local Anesthetic ◽  
Nervous Activity ◽  
Smooth Muscles ◽  
Vagus Nerves ◽  
Cough Reflex ◽  
Bupivacaine Hydrochloride ◽  
Anesthetized Dogs ◽  
Respiratory Reflexes ◽  
Stimulation Of

The effects of inhalation of 100 breaths of bupivacaine hydrochloride (5 percent solution in saline) on the cough reflex, the Breuer-Hering inflation, reflex, and the duration of apnea and bronchoconstriction produced by histamine aerosol were studied in nine anesthetized dogs. Cough was abolished in every animal; the duration of the inflation reflex was shortened from 47 +/- 4.6 s (mean plus or minus SE) to 16 +/- 3.4 s. The duration apnea produced by histamine was abolished or shortened and the rise in resistance was diminished from 170 plus or minus 22 per cent (control) to 49 +/- 6 per cent (after bupivacaine). These reflexes returned toward control values within 45 min. Bupivacaine inhibited the bronchoconstriction produced by electrical stimulation of the distal ends of cut vagus nerves both in dogs and in rabbits, but it did not alter the rise in resistance produced by histamine aerosol in vagotomized dogs. We conclude that administration of bupivacaine aerosol produces a reversible blockage of both afferent and efferent nervous activity in airways without abolishing the ability of smooth muscles to contract.

Vagal feedback with expiratory threshold load under extracorporeal circulation

1983 ◽  
Vol 55 (2) ◽  
pp. 316-322 ◽  
Author(s):  
Y. Jammes ◽  
P. T. Bye ◽  
R. L. Pardy ◽  
C. Roussos
Keyword(s):  
Extracorporeal Circulation ◽  
Vagal Stimulation ◽  
Inhibitory Response ◽  
Vagal Afferents ◽  
Vagus Nerves ◽  
Anesthetized Dogs ◽  
Expiratory Muscles ◽  
Evoked Activity ◽  
Proprioceptive Inputs ◽  
Stimulation Of

In 11 anesthetized dogs placed under extracorporeal circulation, the vagal feedback was tested by electrical stimulation of the vagus nerves with cold block of their caudal part and by passive lung hyperinflation. The apneic response to such vagal stimulation progressively disappeared during expiratory threshold load breathing but then returned to control values some minutes after the load was removed. This suppression of the inhibitory response to stimulation of the vagus nerves was usually observed when vagal afferents were intact or blocked by cold. However, it was not observed whether no evoked activity continued in expiratory muscles after the cold block, or after suppression of all proprioceptive muscular afferents after transection of the spinal cord at C6 level. These results strongly suggest that enhancement of proprioceptive inputs to the respiratory centers counteracts the vagally mediated inspiratory “off-switch” mechanisms.

Nonuniform Distribution of Vagal Effects on the Atrial Refractory Period

1958 ◽  
Vol 194 (2) ◽  
pp. 406-410 ◽  
Author(s):  
R. Alessi ◽  
M. Nusynowitz ◽  
J. A. Abildskov ◽  
G. K. Moe
Keyword(s):  
Arterial Pressure ◽  
Refractory Period ◽  
Vagal Stimulation ◽  
Nonuniform Distribution ◽  
Right Atrial ◽  
Vagus Nerves ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

The refractory period (RP) was measured at several points on the right atrial surface in anesthetized dogs. Under control conditions with vagi cut the values recorded at various points varied by no more than 40 msec. During stimulation of the vagus nerves, singly or together, the RP varied widely. At some points marked effects were observed, while at others little or no effect was apparent. Reflex excitation of the vagi, induced by increased arterial pressure, yielded similar results. It was concluded that the effects of vagal stimulation are not uniformly distributed.

Somatostatin restraint of gastrin secretion in pigs revealed by monoclonal antibody immunoneutralization

1992 ◽  
Vol 263 (6) ◽  
pp. G908-G912 ◽  
Author(s):  
J. J. Holst ◽  
P. N. Jorgensen ◽  
T. N. Rasmussen ◽  
P. Schmidt
Keyword(s):  
Monoclonal Antibody ◽  
Electrical Stimulation ◽  
Vagal Stimulation ◽  
Binding Capacity ◽  
Functional Coupling ◽  
Vagus Nerves ◽  
Basal Secretion ◽  
Gastrin Cells ◽  
Gastrin Secretion ◽  
Stimulation Of

We studied the functional coupling between antral somatostatin and gastrin cells in isolated perfused porcine antrum using immunoneutralization with monoclonal antibodies against somatostatin. Their binding affinity was 10(11) l/mol, and the final binding capacity was 11.7 nmol/ml. Antibody infusion within 1 min increased gastrin secretion, reaching a rate of 349 +/- 64% (means +/- SE, n = 7) of basal secretion (59 +/- 5 pmol/l) after 5 min. The effect of somatostatin at 10(-9) mol/l, which inhibited gastrin secretion from 58 +/- 11 to 14 +/- 3 pmol/min (n = 4), was abolished by antibody infusion. Electrical stimulation of the vagus nerves (n = 7) performed during antibody infusion increased gastrin secretion from 224 +/- 61 to 328 +/- 55 pmol/min, not significantly different from the increase in control experiments from 43 +/- 9 to 118 +/- 20 pmol/min, indicating that the vagal stimulation of gastrin secretion does not depend on mechanisms involving somatostatin. We conclude that paracrine antral somatostatin secretion is one of the most important factors regulating basal gastrin secretion in pigs.

Vagal stimulation-induced gastric damage in rats

1991 ◽  
Vol 261 (1) ◽  
pp. G104-G110
Author(s):  
L. E. Hierlihy ◽  
J. L. Wallace ◽  
A. V. Ferguson
Keyword(s):  
Vagal Stimulation ◽  
Mucosal Damage ◽  
Vagal Afferents ◽  
Gastric Damage ◽  
Gastric Mucosal Damage ◽  
Sprague Dawley ◽  
Vagus Nerves ◽  
Sprague Dawley Rats ◽  
Series Of Experiments ◽  
Stimulation Of

The role of the vagus nerve in the development of gastric mucosal damage was examined in urethan-anesthetized male Sprague-Dawley rats. Electrical stimulation was applied to the vagus nerves for a period of 60 min, after which macroscopic gastric damage was scored and samples of the stomach were fixed for later histological assessment. Damage scores were assigned blindly based on a 0 (normal) to 3 (severe) scale. Stimulation of vagal afferents or efferents in isolation did not result in significant damage to the gastric mucosa (P greater than 0.1). In contrast, stimulation of both intact vagus nerves resulted in significant gastric mucosal damage (mean damage score, 2.0 +/- 0.33, P less than 0.01). A second series of experiments demonstrated this gastric damage to be induced within 30-60 min; extending the stimulation period to 120 min did not worsen the gastric damage scores significantly (P greater than 0.1). In a third study, stimulation of both intact vagus nerves after paraventricular nucleus (PVN) lesion resulted in damage scores (0.33 +/- 0.17) that were significantly reduced compared with intact PVN and non-PVN-lesioned animals (P less than 0.01). These results indicate that the development of vagal stimulation-induced gastric damage requires the activation of both afferent and efferent vagal components and suggest further that such damage is dependent upon an intact PVN.

Pulmonary C-fibers reflexly increase secretion by tracheal submucosal glands in dogs

1985 ◽  
Vol 58 (3) ◽  
pp. 907-910 ◽  
Author(s):  
H. D. Schultz ◽  
A. M. Roberts ◽  
C. Bratcher ◽  
H. M. Coleridge ◽  
J. C. Coleridge ◽  
...  
Keyword(s):  
Gland Secretion ◽  
Right Atrial ◽  
Vagus Nerves ◽  
C Fibers ◽  
Airway Secretion ◽  
Submucosal Glands ◽  
C Fiber ◽  
Anesthetized Dogs ◽  
The Right ◽  
Stimulation Of

Stimulation of bronchial C-fibers evokes a reflex increase in secretion by tracheal submucosal glands, but the influence of pulmonary C-fibers on tracheal gland secretion is uncertain. In anesthetized dogs with open chests, we sprayed powdered tantalum on the exposed mucosa of a segment of the upper trachea to measure the rate of secretion by submucosal glands. Secretions from the gland ducts caused elevations (hillocks) in the tantalum layer. We counted hillocks at 10-s intervals for 60 s before and 60 s after we injected capsaicin (10–20 micrograms/kg) into the right atrium to stimulate pulmonary C-fiber endings. Right atrial injection of capsaicin increased the rate of hillock formation fourfold, but left atrial injection had no significant effect. The response was abolished by cutting the vagus nerves or cooling them to 0 degree C. We conclude that the reflex increase in tracheal submucosal gland secretion evoked by right atrial injection of capsaicin was initiated as capsaicin passed through the pulmonary vascular bed, and hence that pulmonary C-fibers, like bronchial C-fibers, reflexly increase airway secretion.

Afferent vagal stimulation, vasopressin, and nitroprusside alter cerebrospinal fluid kinin

1987 ◽  
Vol 253 (1) ◽  
pp. R136-R141 ◽  
Author(s):  
G. R. Thomas ◽  
H. Thibodeaux ◽  
H. S. Margolius ◽  
J. G. Webb ◽  
P. J. Privitera
Keyword(s):  
Cerebrospinal Fluid ◽  
Vagal Stimulation ◽  
Cardiovascular Regulation ◽  
Perfusion System ◽  
Ventriculocisternal Perfusion ◽  
Anesthetized Dogs ◽  
Bilateral Vagotomy ◽  
Afferent Vagal ◽  
Nitroprusside Infusion ◽  
Stimulation Of

The effects of afferent vagal stimulation, cerebroventricular vasopressin, and intravenous nitroprusside on cerebrospinal fluid (CSF) kinin levels, mean arterial pressure (MAP), and heart rate (HR) were determined in anesthetized dogs in which a ventriculocisternal perfusion system (VP) was established. Following bilateral vagotomy, stimulation of the central ends of both vagi for 60 min significantly increased MAP and CSF perfusate levels of kinin and norepinephrine (NE). MAP was increased a maximum of 32 +/- 4 mmHg, and the rates of kinin and NE appearance into the CSF perfusate increased from 4.2 +/- 1.4 to 22.1 +/- 6.9 and from 28 +/- 5 to 256 +/- 39 pg/min, respectively. A significant correlation was found between CSF kinin and NE levels in these experiments. In other experiments the addition of arginine vasopressin to the VP system caused a significant increase in CSF perfusate kinin without affecting MAP or HR. Intravenous infusion of nitroprusside lowered MAP without affecting kinin levels in the CSF. However, on cessation of nitroprusside infusion, CSF kinin increased significantly in association with the return in MAP to predrug level. Collectively the data are consistent with the hypothesis that central nervous system kinins have some role in cardiovascular regulation, and furthermore that this role may involve an interaction between brain kinin and central noradrenergic neuronal pathways.

Sign in / Sign up

Export Citation Format

Share Document