Inspiratory inhibition and rebound activation elicited by intermittent electrical bulbar stimulation in various states of pulmonary afferent vagal excitation

1975 ◽  
Vol 357 (1-2) ◽  
pp. 123-138 ◽  
Author(s):  
Marc Fallert ◽  
Christine Spillmann
Keyword(s):  
Bulbar Stimulation ◽  
Afferent Vagal

Chemical afferent vagal axotomy blocks re-intake after partial withdrawal of gastric food contents

2016 ◽  
Vol 20 (10) ◽  
pp. 587-597 ◽  
Author(s):  
María A. Zafra ◽  
Filomena Molina ◽  
Amadeo Puerto
Keyword(s):  
Afferent Vagal

Meal-synchronized CEA in rats: effects of meal size, intragastric feeding, and subdiaphragmatic vagotomy

1999 ◽  
Vol 276 (5) ◽  
pp. R1276-R1288 ◽  
Author(s):  
Wesley White ◽  
Gary J. Schwartz ◽  
Timothy H. Moran
Keyword(s):  
Meal Size ◽  
Vagal Activity ◽  
Subdiaphragmatic Vagotomy ◽  
Feeding Cycle ◽  
Induce Activity ◽  
Before And After ◽  
Afferent Vagal ◽  
G 34 ◽  
Nutrient Infusion ◽  
Intact Rats

Within a feeding schedule of intermittent food access, large meals have the ability to induce activity at the same time the next day [circadian ensuing activity (CEA)]. In these experiments, we evaluated the minimum meal size necessary to induce CEA and whether oral-pharyngeal factors and afferent vagal activity played necessary roles in the induction of the underlying process. In experiment 1, every 33 h rats were given two meals separated by a 2-h interval. The size of the first meal was varied, while total intake every feeding cycle was held constant. When the initial meal was <10 g (34 kcal) CEA occurred later, indicating that such a meal size was subthreshold for inducing CEA. In experiment 2, rats were given intragastric (IG) meals every 33 h, before and after complete subdiaphragmatic vagotomy. IG nutrient meals induced CEA, indicating that extensive oral-pharyngeal experience was not necessary for CEA induction. CEA occurred in vagotomized rats but, compared with intact rats, appeared to occur later relative to nutrient infusion, indicating that afferent vagal activity may be sufficient but not necessary to induce CEA.

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.

Role of vagal afferents in the control of abdominal expiratory muscle activity in the dog

1991 ◽  
Vol 71 (5) ◽  
pp. 1795-1800 ◽  
Author(s):  
S. B. Hollstien ◽  
M. L. Carl ◽  
E. S. Schelegle ◽  
J. F. Green
Keyword(s):  
Muscle Activity ◽  
Vagal Afferents ◽  
Oblique Muscle ◽  
Vagus Nerves ◽  
Expiratory Muscle ◽  
C Fibers ◽  
C Fiber ◽  
Before And After ◽  
Afferent Vagal ◽  
Alpha Chloralose

We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.

Medullary afferent vagal axotomy disrupts NaCl-induced short-term taste aversion learning

1993 ◽  
Vol 59 (1) ◽  
pp. 69-75 ◽  
Author(s):  
M. Arnedo ◽  
M. Gallo ◽  
A. Aguero ◽  
F. Molina ◽  
A. Puerto
Keyword(s):  
Taste Aversion ◽  
Aversion Learning ◽  
Short Term ◽  
Taste Aversion Learning ◽  
Afferent Vagal

scholarly journals An Afferent Vagal Nerve Pathway Links Hepatic PPARα Activation to Glucocorticoid-Induced Insulin Resistance and Hypertension

2007 ◽  
Vol 5 (2) ◽  
pp. 91-102 ◽  
Author(s):  
Carlos Bernal-Mizrachi ◽  
Liu Xiaozhong ◽  
Li Yin ◽  
Russell H. Knutsen ◽  
Michael J. Howard ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Vagal Nerve ◽  
Afferent Vagal

THE EFFECT OF VAGOTOMY AND DENERVATION OF THE CAROTID SINUS ON DIURESIS FOLLOWING PLASMA VOLUME EXPANSION

1959 ◽  
Vol 37 (1) ◽  
pp. 81-90 ◽  
Author(s):  
J. W. Pearce
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Carotid Sinus ◽  
Urine Flow ◽  
Flow Section ◽  
Plasma Volume Expansion ◽  
Reflex Mechanism ◽  
Albumin Infusion ◽  
Stretch Receptors ◽  
Afferent Vagal

The hypothesis exists that afferent vagal fibers, arising in cardiac atrial stretch receptors, serve as the sensory limb of a reflex mechanism sensitive to variations in blood volume and producing corresponding changes in urine flow. Section of the vagi did not, however, prevent the diuretic and chloruretic response to expansion of the plasma volume with isotonic infusions. Carotid sinus denervation alone or combined with vagotomy also failed to prevent the diuresis and chloruresis following infusion in most experiments, although in a few cases the response was absent or diminished after the combined procedure. Reasons are given for believing that the bovine albumin infusion used did not act directly on the kidney to increase urine output, but rather through a reflex mechanism which could not have depended on the integrity of the vagi. It is concluded that receptors additional to those in the cardiac atria and the carotid sinus must contribute to the sensory component of a reflex mechanism regulating plasma volume.

Sign in / Sign up

Export Citation Format

Share Document