Selective AV nodal vagal stimulation improves hemodynamics during acute atrial fibrillation in dogs

2001 ◽  
Vol 281 (4) ◽  
pp. H1490-H1497 ◽  
Author(s):  
Don W. Wallick ◽  
Youhua Zhang ◽  
Tomotsugu Tabata ◽  
Shaowei Zhuang ◽  
Kent A. Mowrey ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Nerve Stimulation ◽  
Atrioventricular Node ◽  
Vital Role ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Ventricular Rate ◽  
Significant Deterioration ◽  
Vagal Nerves

Although the atrioventricular node (AVN) plays a vital role in blocking many of the atrial impulses from reaching the ventricles during atrial fibrillation (AF), a rapid irregular ventricular rate nevertheless persists. The goals of the present study were to explore the feasibility of novel epicardial selective vagal nerve stimulation for slowing of the ventricular rate during AF and to characterize the hemodynamic benefits in vivo. Electrophysiological-echocardiographic experiments were performed on 11 anesthetized open-chest dogs. Hemodynamic measurements were performed during three distinct periods: 1) sinus rate, 2) AF, and 3) AF with vagal nerve stimulation. AF was associated with significant deterioration of all measured parameters ( P < 0.025). The vagal nerve stimulation produced slowing of the ventricular rate, significant reversal of the pressure and contractile indexes ( P < 0.025), and a sharp reduction in one-half of the abortive ventricular contractions. The present study provides comprehensive evidence that slowing of the ventricular rate during AF by selective ganglionic stimulation of the vagal nerves that innervate the AVN successfully improved the hemodynamic responses.

In vivo detection of endogenous acetylcholine release in cat ventricles

1994 ◽  
Vol 266 (3) ◽  
pp. H854-H860 ◽  
Author(s):  
T. Akiyama ◽  
T. Yamazaki ◽  
I. Ninomiya
Keyword(s):  
Nerve Stimulation ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Left Ventricular Myocardium ◽  
Ach Release ◽  
Vagal Nerves ◽  
Dialysis Technique

To detect and monitor endogenous acetylcholine (ACh) release in the in vivo heart, we applied a dialysis technique to the hearts of anesthetized cats. Dialysis probes were implanted in the left ventricular myocardium and were perfused with Krebs-Henseleit solution containing Eserine (10(-4) M) at 3 microliters/min. Dialysate ACh concentration was measured with high-performance liquid chromatography. In four cats, the response to vagal stimulation was studied. Electrical stimulation of efferent vagal nerves (10 Hz) significantly increased dialysate ACh concentration from 596 +/- 118 (control) to 12,210 +/- 1,661 pM. After stimulation, dialysate ACh concentration significantly decreased to 382 +/- 80 pM below control. The influence of ganglionic blocker was determined in six cats. Control vagal nerve stimulation (10 Hz) increased dialysate ACh concentration from 582 +/- 136 to 9,102 +/- 754 pM. Local perfusion of hexamethonium (10(-4) M) did not affect this nerve stimulation-induced ACh increase (8,611 +/- 1,189 pM), and intravenous administration of hexamethonium (20 mg/kg) prevented this increase (340 +/- 88 pM). We examined the response to vagal nerve stimulation at different frequencies in three cats. Vagal nerve stimulation increased dialysate ACh concentration from a control of 588 +/- 211 to 1,227 +/- 195 pM at 2 Hz, 3,946 +/- 1,059 pM at 5 Hz, and 9,366 +/- 1,873 pM at 10 Hz. Dialysate ACh concentration reflects ACh release from postganglionic vagal nerves innervating the left ventricular myocardium; the dialysis technique permits estimation of relative changes in efferent cardiac vagal nerve activity.

Vagal nerve stimulation causes noncholinergic dilatation of gastric arterioles

1986 ◽  
Vol 250 (5) ◽  
pp. G660-G664
Author(s):  
T. Morishita ◽  
P. H. Guth
Keyword(s):  
Blood Flow ◽  
Nerve Stimulation ◽  
Mucosal Blood Flow ◽  
Gastric Mucosal Blood Flow ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
In Vivo Microscopy ◽  
Vasodilator Effect ◽  
Splitting Technique

Vagal nerve stimulation causes prompt dilatation of gastric submucosal arterioles (the vessels that control gastric mucosal blood flow) in rats. In vivo microscopy was used to determine whether this direct vasodilator effect of vagal nerve stimulation on rat gastric submucosal arterioles is mediated by cholinergic fibers. Acetylcholine and atropine were topically applied to the submucosa. The distal end of the severed vagus nerve was electrically stimulated (8 V, 2 ms, 6 Hz, 20 s) subdiaphragmatically. Diameter changes of the submucosal arterioles were videotaped and measured with an image-splitting technique on playback of the videotapes. Acetylcholine, 10(-7) to 10(-5) M, dilated the arterioles dose dependently. Atropine prevented the acetylcholine-induced dilatation, 10(-5) M, nearly completely inhibiting the dilatation. Vagal nerve stimulation dilated the arterioles promptly, and this dilatation was not blocked by 10(-5) M atropine, a dose that blocked the acetylcholine-induced dilatation. These results indicate that vagal nerve stimulation causes atropine-resistant, noncholinergic dilatation of gastric submucosal arterioles in rats.

scholarly journals Differences in atrial fibrillation properties under vagal nerve stimulation versus atrial tachycardia remodeling

Heart Rhythm ◽  
2009 ◽  
Vol 6 (10) ◽  
pp. 1465-1472 ◽  
Author(s):  
Grigorios Katsouras ◽  
Masao Sakabe ◽  
Philippe Comtois ◽  
Ange Maguy ◽  
Brett Burstein ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Nerve Stimulation ◽  
Atrial Tachycardia ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation

scholarly journals Effect of Bepridil in Atrial Fibrillation Inducibility Facilitated by Vagal Nerve Stimulation

2010 ◽  
Vol 74 (5) ◽  
pp. 895-902 ◽  
Author(s):  
Kenichi Iijima ◽  
Masaomi Chinushi ◽  
Daisuke Izumi ◽  
Shizue Ahara ◽  
Hiroshi Furushima ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Nerve Stimulation ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation

scholarly journals EFEKTIVITAS VAGAL NERVE STIMULATION (VNS) TERHADAP DISRITMIA JANTUNG

2020 ◽  
Vol 2 (01) ◽  
pp. 7-20
Author(s):  
Pius A. L. Berek
Keyword(s):  
Atrial Fibrillation ◽  
Vagus Nerve ◽  
Nerve Stimulation ◽  
Carotid Sinus ◽  
Electrical Conductance ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Av Node ◽  
Sa Node ◽  
Release Of Acetylcholine

Dysrhythmia is a heart rate disorder that includes frequency or rhythm disorders or both. One of the nursing actions to overcome is doing Vagal Nerve Stimulation (VNS), includes emphasis on one side of carotid sinus, emphasis on periorbital sinus, and performing valsalava maneuver by coughing. This is believed to increase release of acetylcholine in heart, where the acetylcholine is captured by SA node in left atrium and serves as an inhibitor of electrical stimulation of heart. The release of acetylcholine production is expected to inhibit cardiac irritability so ventricular contraction can be reduced to a minimum. This will appear clearly in state of dysrhythmias, especially atrial fibrillation. In atrial fibrillation, the impulses produced in atrium will exceed normal state, which results in electrical conductance of heart to SA node, continued to AV node and to purkinje fibers to increase ventricular contractions in projecting blood out of heart. If the impulses produced by atrium are irregular, the same thing happens to ventricles, which is to make irregular heart contractions as well. The result is the heart does not have time to relax to give blood to coronary arteries. If not handled properly, this is very dangerous for heart. VNS action by providing stimulation to vagus nerve will greatly help overcome this problem because the ends of the vagus nerve lead to SA node and AV node. By providing stimulation to vagus nerve, the signal will be sent to efferent to release ACh. It is hoped that this ACh will inhibit impulses from SA node and AV node so the heart can contract according to the body's needs.

High Density Mapping of Atrial Fibrillation During Vagal Nerve Stimulation in the Canine Heart: Restudying the Moe Hypothesis

2012 ◽  
Vol 24 (3) ◽  
pp. 328-335 ◽  
Author(s):  
SEUNGYUP LEE ◽  
JAYAKUMAR SAHADEVAN ◽  
CELEEN M. KHRESTIAN ◽  
DOMINIQUE M. DURAND ◽  
ALBERT L. WALDO
Keyword(s):  
Atrial Fibrillation ◽  
Nerve Stimulation ◽  
High Density ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Canine Heart ◽  
Density Mapping

Effect and mechanism of vagal nerve stimulation on somatostatin secretion in dogs

1986 ◽  
Vol 250 (2) ◽  
pp. E212-E217 ◽  
Author(s):  
B. Ahren ◽  
T. L. Paquette ◽  
G. J. Taborsky
Keyword(s):  
Electrical Stimulation ◽  
Nerve Stimulation ◽  
Nicotinic Receptors ◽  
Vagal Nerve ◽  
Vagal Nerve Stimulation ◽  
Base Line ◽  
Anesthetized Dogs ◽  
Arterial Plasma ◽  
Stimulation Of

To investigate the effect of vagal nerve stimulation on the release of pancreatic somatostatin, we electrically stimulated (10 Hz, 5 ms, 13.5 mA, and 10 min) the thoracic vagi just below the heart in halothane anesthetized dogs (n = 15). The stimulation increased the pancreatic output of somatostatinlike immunoreactivity (SLI) (delta = +248 +/- 81 fmol/min, P less than 0.005; base-line levels = 455 +/- 150 fmol/min). min). Arterial plasma SLI levels increased as well (delta = +16 +/- 3 fmol/ml, P less than 0.001; base-line levels = 65 +/- 3 fmol/ml), reflecting stimulation of extrapancreatic SLI secretion. Significant vagal activation was verified by a fivefold increase of pancreatic output of pancreatic polypeptide (PP) (delta = +31.4 +/- 5.9 ng/min, P less than 0.001; base-line levels = 7.8 +/- 0.9 ng/min). Atropine pretreatment (n = 6) inhibited partially both the PP response (delta = +7.9 +/- 3.8 ng/min after atropine) and the pancreatic SLI response (delta = +92 +/- 29 fmol/min) to vagal nerve stimulation. However, atropine pretreatment did not modify the arterial SLI response (delta = +20 +/- 7 fmol/ml). Hexamethonium pretreatment (n = 9) completely abolished all three responses. We conclude that 1) electrical stimulation of the vagus stimulates pancreatic SLI, extrapancreatic SLI, and PP release in vivo in the dog; 2) both muscarinic and nonmuscarinic mechanisms mediate the PP and pancreatic SLI responses; 3) a nonmuscarinic mechanism mediates the extrapancreatic SLI response; and 4) all three responses are mediated via ganglionic nicotinic receptors.

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