Effect of stimulation of vagus nerves on gastric tissue histamine concentration in albino rats

1979 ◽  
Vol 35 (1) ◽  
pp. 54-55 ◽  
Author(s):  
A. K. Ganguly ◽  
P. Gopinath
Keyword(s):  
Albino Rats ◽  
Gastric Tissue ◽  
Vagus Nerves ◽  
Histamine Concentration ◽  
Tissue Histamine ◽  
Stimulation Of

Effect of daily parenteral injection of betamethasone on histamine concentration of gastric tissue in albino rats

1980 ◽  
Vol 36 (8) ◽  
pp. 979-980
Author(s):  
A. K. Ganguly ◽  
K. Somasundaram ◽  
R. H. Majithia ◽  
V. K. Chawla
Keyword(s):  
Albino Rats ◽  
Gastric Tissue ◽  
Histamine Concentration ◽  
Parenteral Injection

scholarly journals Post-activation potentiation of gastric and intestinal contractions in response to stimulation of the vagus nerves

1959 ◽  
Vol 148 (2) ◽  
pp. 437-449 ◽  
Author(s):  
E. L. Blair ◽  
A. A. Harper ◽  
C. Kidd ◽  
T. Scratcherd
Keyword(s):  
Vagus Nerves ◽  
Stimulation Of

Dysfunction of M2-muscarinic receptors in pulmonary parasympathetic nerves after antigen challenge

1991 ◽  
Vol 71 (6) ◽  
pp. 2255-2261 ◽  
Author(s):  
A. D. Fryer ◽  
M. Wills-Karp
Keyword(s):  
Muscarinic Receptors ◽  
Guinea Pigs ◽  
Antigen Challenge ◽  
Saline Control ◽  
Control Group ◽  
Vagus Nerves ◽  
Parasympathetic Nerves ◽  
Volume Blood ◽  
M2 Muscarinic Receptors ◽  
Stimulation Of

The effect of antigen challenge on the function of neuronal M2-muscarinic autoreceptors in the lungs was studied in anesthetized guinea pigs. Guinea pigs were injected intraperitoneally with saline (control group) or ovalbumin (10 mg/kg) on days 1, 3, and 5. One group of sensitized animals was challenged on days 20–25 with aerosolized ovalbumin for 5 min/day (challenged group), while another group of the sensitized animals was not challenged (sensitized group). On day 26 the animals were anesthetized, paralyzed, tracheostomized, and artificially ventilated. Pulmonary inflation pressure (Ppi), tidal volume, blood pressure, and heart rate were recorded. Both vagus nerves were cut, and electrical stimulation of the distal portions caused bronchoconstriction (measured as an increase in Ppi) and bradycardia. In the control group, pilocarpine (1–100 micrograms/kg iv) attenuated vagally induced bronchoconstriction by stimulating inhibitory M2-muscarinic receptors on parasympathetic nerves in the lungs. Conversely, blockade of these receptors with the antagonist gallamine (0.1–10 mg/kg iv) produced a marked potentiation of vagally induced bronchoconstriction. These results confirm previous findings. In the challenged guinea pigs, pilocarpine did not inhibit vagally induced bronchoconstriction. Furthermore, gallamine did not potentiate vagally induced bronchoconstriction to the same degree as in the controls. In the group of animals that was sensitized but not challenged, the potentiation of vagally induced bronchoconstriction by gallamine was identical to the controls. There was no increase in baseline Ppi in the sensitized or challenged animals compared with the controls.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

scholarly journals Effect of Duloxetine Pretreatment on 5-HTP and Dexfenfluramine Induced Behaviours in Albino Rats

2019 ◽  
Vol 12 (3) ◽  
pp. 1339-1343
Author(s):  
Vandana Milind Thorat ◽  
Chitra C Khanwelkar ◽  
Somnath Mallikarjun Matule ◽  
Pratibha Satish Salve ◽  
Smita Ajit Surle-Patil ◽  
...  
Keyword(s):  
Serotonin Transporter ◽  
Behavioural Syndrome ◽  
Albino Rats ◽  
Behavioral Syndrome ◽  
Serotonergic Receptors ◽  
Central Brain ◽  
Pre Treatment ◽  
Stimulation Of

Activation of central brain serotonergic receptors viz 5-HT1A and 5-HT2A by serotonin (5-HT) induces the 5-HT behavioural syndrome in rats. 5-HTP and dexfenfluramine produce 5-HT mediated behaviours. We have carried out the experiment with the aim to study the effect of duloxetine pretreatment on 5-hydroxytryptophan and dexfenfluramine induced behaviours in albino rats. Pre-treatment with 20 mg/kg duloxetine, a SNRI was found to potentiate 75 mg/kg 5-HTP mediated behavioural syndrome. However, 5, 10 and 20 mg/kg duloxetine had decreased the intensity of the behavioral syndrome produced by 10 mg/kg dexfenfluramine significantly. Duloxetine at 5, 10 and 20 mg/kg had produced inhibition of serotonin transporter (SERT) and inhibited dexfenfluramine uptake which had significantly antagonised its behavioural syndrome. Duloxetine at 5 and 10 mg/kg did not affect 5-HTP induced behavioral syndrome significantly where as 20 mg/kg duloxetine did significantly potentiate 5-HTP induced behavioral syndrome. This indicates 20 mg/kg dose of duloxetine blocks neuronal reuptake of 5-HT by blocking SERT and effectively increase its concentration to greater level in the synaptic gap which causes synergistic stimulation of the central postsynaptic 5-HT1A and 5-HT2A receptors and potentiation of 5-HTP behavioral syndrome.

scholarly journals THE INFLUENCE OF THE VAGUS NERVES UPON CONDUCTION BETWEEN AURICLES AND VENTRICLES IN THE DOG DURING AURICULAR FIBRILLATION

1916 ◽  
Vol 24 (5) ◽  
pp. 605-619 ◽  
Author(s):  
G. Canby Robinson
Keyword(s):  
Vagus Nerve ◽  
Vagus Nerves ◽  
The Right ◽  
Left Vagus ◽  
Stimulation Of

The experiments that have been reported indicate that stimulation of either the right vagus or the left vagus nerve is equally effectual in blocking impulses from the auricles to the ventricles when auricular fibrillation is present. Stimulation of the left vagus nerve is as effectual in blocking impulses from the normally beating auricles as from the auricles when in a state of fibrillation, and the type of auricular activity has apparently no influence on the effect which stimulation of the left vagus has on auriculoventricular conduction.

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.

Gastrin-releasing peptide: effect on exocrine secretion and release from isolated perfused porcine pancreas

1985 ◽  
Vol 248 (3) ◽  
pp. G281-G286 ◽  
Author(s):  
S. Knuhtsen ◽  
J. J. Holst ◽  
S. L. Jensen ◽  
U. Knigge ◽  
O. V. Nielsen
Keyword(s):  
Exocrine Secretion ◽  
Arterial Line ◽  
Pancreatic Exocrine Secretion ◽  
Vagus Nerves ◽  
Porcine Pancreas ◽  
Gastrin Releasing Peptide ◽  
Atropine Treatment ◽  
Pancreatic Exocrine ◽  
Control Fluid ◽  
Stimulation Of

The effect of gastrin-releasing peptide (GRP) on pancreatic exocrine secretion was studied by infusing it at four dose levels (0.01, 0.1, 1.0, and 10 nmol/l) into the arterial line of the isolated perfused porcine pancreas. At 1.0 nmol/l GRP stimulated protein (37-fold), fluid (13-fold), and bicarbonate secretion (12-fold). Atropine at 1 mumol/l diminished the protein secretion in response to infusion of GRP at a dose of 1 nmol/l to 45% of control. Fluid and bicarbonate responses were not affected by atropine treatment. Electrical stimulation of the vagus nerves resulted in an increase in pancreatic output of GRP and a concomitant stimulation of exocrine secretion. Infusions of acetylcholine, carbachol, pilocarpine, or dimethylphenylpiperazinium had no effect on the output of GRP, although hexamethonium abolished the response to vagal stimulation. It is concluded that GRP in conjunction with acetylcholine is likely to play a prominent part in parasympathetic regulation of pancreatic exocrine secretion.

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