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.

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.

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.

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.

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.

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.

Responses of medullary raphespinal neurons to electrical stimulation of thoracic sympathetic afferents, vagal afferents, and to other sensory inputs in cats

1991 ◽  
Vol 66 (6) ◽  
pp. 2084-2094 ◽  
Author(s):  
R. W. Blair ◽  
A. R. Evans
Keyword(s):  
Electrical Stimulation ◽  
Neuronal Activity ◽  
Vagal Stimulation ◽  
Discharge Rate ◽  
Stellate Ganglion ◽  
Cell Activity ◽  
Conditioning Stimulus ◽  
Vagal Afferents ◽  
Early Peak ◽  
Stimulation Of

1. Medullary raphespinal neurons antidromically activated from the T2-T5 segments were tested for responses to electrical stimulation of cervical vagal and thoracic sympathetic afferents (by stimulating the left stellate ganglion), somatic probing, auditory stimuli, and visual stimuli in cats anesthetized with alpha-chloralose. A total of 99 neurons in the raphe nuclei were studied; the locations of 76 cells were histologically confirmed. Neurons were located in raphe magnus (RM, 65%), raphe obscurus (RO, 32%), and raphe pallidus (RPa, 4%). The mean conduction velocity of these neurons was 62 +/- 2.9 (SE) m/s with a range of 1.1-121 m/s. 2. A total of 60/99 tested neurons responded to electrical stimulation of sympathetic afferents. Quantitation of responses was obtained for 55 neurons. With one exception, all responsive neurons were excited and exhibited an early burst of spikes with a mean latency of 16 +/- 1.2 ms. From a spontaneous discharge rate of 5.2 +/- 1.2 spikes/s, neuronal activity increased by 2.9 +/- 0.3 spikes/stimulus. In addition to an early peak, 15 neurons (25%) exhibited a late burst of spikes with a latency of 182 +/- 12.9 ms; neuronal activity increased by 5.0 +/- 1.3 spikes/stimulus. Duration of the late peak (130 +/- 18.5 ms) was longer than for the early peak (18 +/- 0.7 ms), but threshold voltages for eliciting each peak were comparable. Sixteen of 29 spontaneously active neurons exhibited a postexcitatory depression of activity that lasted for 163 +/- 19.1 ms. All but one tested neuron in RO responded to stimulation of sympathetic afferents, but 65% of neurons in RM responded to this stimulus. 3. In response to vagal afferent stimulation, 19% of 57 neurons exhibited inhibition only, 11% were only excited, and 9% were either excited or inhibited, depending on the stimulus paradigm used; the remaining 61% of neurons were unresponsive. From a spontaneous rate of 7.9 +/- 3.8 spikes/s, excited cells increased their discharge rate by 1.6 +/- 0.3 spikes/stimulus. Activity of inhibited cells was reduced from 21.3 +/- 5.8 to 7.8 +/- 3.1 spikes/s. The conditioning-test (CT) technique was used to assess 11 neurons' responses. Stellate ganglion stimulation was the test stimulus, and vagal stimulation the conditioning stimulus. Vagal stimulation reduced the neuronal responses to stellate ganglion stimulation by an average of 50% with a CT interval of 60-100 ms, and cell responses returned to control after 300 ms. With spontaneous cell activity, low frequencies of vagal stimulation were generally excitatory, and high frequencies (10-20 Hz) inhibitory.(ABSTRACT TRUNCATED AT 400 WORDS)

Expiratory threshold load under extracorporeal circulation: effects of vagal afferents

1983 ◽  
Vol 55 (2) ◽  
pp. 307-315 ◽  
Author(s):  
Y. Jammes ◽  
P. T. Bye ◽  
R. L. Pardy ◽  
C. Katsardis ◽  
S. Esau ◽  
...  
Keyword(s):  
Mechanical Vibration ◽  
Muscle Spindles ◽  
Vagal Afferents ◽  
Abdominal Muscles ◽  
Vagus Nerves ◽  
Linea Alba ◽  
Arterial Blood Gas ◽  
Arterial Blood ◽  
Anesthetized Dogs ◽  
Proprioceptive Afferents

Nine anesthetized dogs breathed against an expiratory threshold load (ETL) applied by switching the expiratory circuit into a column of H2O to a depth of 20-30 cm. Arterial blood gas tensions were maintained in the normal range by placing the dogs under arteriovenous bypass to avoid any uncontrolled chemostimulation. There was an increase in integrated electromyogram activity of the diaphragm with the ETL. This was rarely observed after cold block of the vagus nerves which also reduced the evoked expiratory activity. The ventilatory response to hypercapnia was greatly depressed under loaded breathing whether vagal afferents were intact or blocked by cold. Both inspiratory drive and ventilatory timing were affected, suggesting that the central integration of chemosensitive afferents was altered. Proof of supraspinal projections of proprioceptive inputs from abdominal muscles was provided by the demonstration of changes in ventilatory timing during selective activation of muscle spindles in abdominal muscles by high-frequency mechanical vibration applied to the linea alba. Thus these observations suggest that during ETL breathing, a possible interaction exists between chemoreflex drive and proprioceptive afferents.

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.

Mechanisms of action of sodium cromoglycate

1985 ◽  
Vol 63 (6) ◽  
pp. 760-765 ◽  
Author(s):  
D. F. Biggs ◽  
V. Goel
Keyword(s):  
Blood Pressure ◽  
Sodium Cromoglycate ◽  
Arterial Blood Pressure ◽  
Vagal Stimulation ◽  
Cardiovascular Responses ◽  
Bilateral Stimulation ◽  
Vagus Nerves ◽  
Arterial Blood ◽  
Efferent Pathways ◽  
Stimulation Of

The effects of sodium cromoglycate (SCG) on cardiovascular and pulmonary responses to phenylbiguanide, capsaicin, and vagal stimulation were studied in anesthetized guinea pigs. Phenylbiguanide had no bronchospastic activity but induced reflex changes in arterial blood pressure which were reduced or abolished by SCG. Capsaicin induced nonreflex bronchospasm, and decreases in arterial blood pressure that were unaffected by SCG. Sodium cromoglycate, given before or after atropine, had no effect on the bronchospasm and cardiovascular responses to unilateral or bilateral stimulation of the vagus nerves. We conclude that SCG may influence both the afferent and efferent pathways of responses to drugs.

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