scholarly journals Intermittent electrical stimulation of the right cervical vagus nerve in salt-sensitive hypertensive rats: effects on blood pressure, arrhythmias, and ventricular electrophysiology

2015 ◽  
Vol 3 (8) ◽  
pp. e12476 ◽  
Author(s):  
Elizabeth M. Annoni ◽  
Xueyi Xie ◽  
Steven W. Lee ◽  
Imad Libbus ◽  
Bruce H. KenKnight ◽  
...  
2002 ◽  
Vol 195 (6) ◽  
pp. 781-788 ◽  
Author(s):  
Thomas R. Bernik ◽  
Steven G. Friedman ◽  
Mahendar Ochani ◽  
Robert DiRaimo ◽  
Luis Ulloa ◽  
...  

Efferent activity in the vagus nerve can prevent endotoxin-induced shock by attenuating tumor necrosis factor (TNF) synthesis. Termed the “cholinergic antiinflammatory pathway,” inhibition of TNF synthesis is dependent on nicotinic α-bungarotoxin-sensitive acetylcholine receptors on macrophages. Vagus nerve firing is also stimulated by CNI-1493, a tetravalent guanylhydrazone molecule that inhibits systemic inflammation. Here, we studied the effects of pharmacological and electrical stimulation of the intact vagus nerve in adult male Lewis rats subjected to endotoxin-induced shock to determine whether intact vagus nerve signaling is required for the antiinflammatory action of CNI-1493. CNI-1493 administered via the intracerebroventricular route was 100,000-fold more effective in suppressing endotoxin-induced TNF release and shock as compared with intravenous dosing. Surgical or chemical vagotomy rendered animals sensitive to TNF release and shock, despite treatment with CNI-1493, indicating that an intact cholinergic antiinflammatory pathway is required for antiinflammatory efficacy in vivo. Electrical stimulation of either the right or left intact vagus nerve conferred significant protection against endotoxin-induced shock, and specifically attenuated serum and myocardial TNF, but not pulmonary TNF synthesis, as compared with sham-operated animals. Together, these results indicate that stimulation of the cholinergic antiinflammatory pathway by either pharmacological or electrical methods can attenuate the systemic inflammatory response to endotoxin-induced shock.


1962 ◽  
Vol 203 (6) ◽  
pp. 1120-1124 ◽  
Author(s):  
John W. Manning ◽  
Marion deV. Cotten

Electrical stimulation of numerous areas in the midbrain reticular formation and in the posterior hypothalamus of the cat increased blood pressure and caused a variety of electrocardiographic changes, including sinus tachycardia, ventricular premature contractions, bigeminal rhythm, A-V dissociation, and ventricular tachycardia. Most commonly, these arrhythmias developed immediately after cessation of diencephalic stimulation but also developed during the period of stimulation in 5 of the 23 cats studied. The arrhythmias disappeared upon cooling and reappeared upon rewarming the vagus nerves. The arrhythmias also were abolished by methylscopolamine, by bilateral vagotomy, or by extirpation of the stellate ganglia. Electrical stimulation of the distal end of the cut right vagus nerve slowed the sinus rate and electrical stimulation of the right stellate ganglion elevated sinus rate, but neither of these procedures caused arrhythmias. Simultaneous stimulation of both the right vagus nerve and the right stellate ganglion, however, caused arrhythmias similar to those observed after diencephalic stimulation. These data are interpreted to indicate that the cardiac arrhythmias evoked by diencephalic stimulation result from the interplay of both sympathetic and parasympathetic influences on the heart.


2017 ◽  
Vol 47 (3) ◽  
pp. 345-351
Author(s):  
S. Yu. Zhilyaev ◽  
A. N. Moskvin ◽  
T. F. Platonova ◽  
I. T. Demchenko

1911 ◽  
Vol 14 (3) ◽  
pp. 217-234 ◽  
Author(s):  
G. Canby Robinson ◽  
George Draper

In hearts showing auricular fibrillation mechanical stimulation of the right vagus nerve causes, as a rule, marked slowing or stoppage of ventricular rhythm, without producing any appreciable effect in the electrocardiographic record of the auricular fibrillation. The ventricular pauses are apparently due to the blocking of stimuli from the auricles. The force of ventricular systole is distinctly weakened for several beats after vagus stimulation, and ectopic ventricular systoles have been seen in several instances, apparently the result of the vagus action. There may, in some cases, be lowered excitability of the ventricles, while no constant change is seen in the size of the electrical complexes representing ventricular systole.


2000 ◽  
Vol 89 (1) ◽  
pp. 139-142 ◽  
Author(s):  
Robert L. Coon ◽  
Patrick J. Mueller ◽  
Philip S. Clifford

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.


2001 ◽  
Vol 91 (4) ◽  
pp. 1713-1722 ◽  
Author(s):  
Fadi Xu ◽  
Tongrong Zhou ◽  
Tonya Gibson ◽  
Donald T. Frazier

Electrical stimulation of the rostral fastigial nucleus (FNr) alters respiration via activation of local neurons. We hypothesized that this FNr-mediated respiratory response was dependent on the integrity of the nucleus gigantocellularis of the medulla (NGC). Electrical stimulation of the FNr in 15 anesthetized and tracheotomized spontaneously breathing rats significantly altered ventilation by 35.2 ± 11.0% ( P < 0.01) with the major effect being excitatory (78%). This respiratory response did not significantly differ from control after lesions of the NGC via bilateral microinjection of kainic or ibotenic acid (4.5 ± 1.9%; P > 0.05) but persisted in sham controls. Eight other rats, in which horseradish peroxidase (HRP) solution was previously microinjected into the left NGC, served as nonstimulation controls or were exposed to either 15-min repeated electrical stimulation of the right FNr or hypercapnia for 90 min. Histochemical and immunocytochemical data showed that the right FNr contained clustered HRP-labeled neurons, most of which were double labeled with c-Fos immunoreactivity in both electrically and CO2-stimulated rats. We conclude that the NGC receives monosynaptic FNr inputs and is required for fully expressing FNr-mediated respiratory responses.


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