Atrial ectopic pacemaker escape mediated by phasic vagal nerve activity

1991 ◽  
Vol 260 (5) ◽  
pp. H1507-H1514 ◽  
Author(s):  
G. J. Rozanski
Keyword(s):  
Cycle Length ◽  
Vagal Nerve ◽  
Vagal Activity ◽  
Drive Cycle ◽  
Nerve Activity ◽  
Vagal Nerve Activity ◽  
Ectopic Pacemaker ◽  
Premature Beats ◽  
Spontaneous Discharges

Effects of vagal nerve activity on atrial ectopic pacemaker foci were studied in vitro in strips of rabbit tricuspid valve. Transmembrane potentials were recorded from pacemaker and working atrial fibers superfused with Tyrode solution containing propranolol. Tissues were paced from the atrial muscle end at cycle lengths of 90, 70, or 50% of the intrinsic pacemaker cycle, and postganglionic vagal nerve endings were stimulated with brief trains of pulses (200 Hz; 100-200 microseconds) through a second electrode near the pacemaker. Vagal trains scanning diastole hyperpolarized pacemaker and surrounding fibers to a maximum membrane potential of -74.7 +/- 1.8 mV (normal maximum diastolic potential = -75.5 +/- 1.6 mV) and elicited a period of inexcitability lasting 217.9 +/- 27.3 ms (drive cycle = 90% of pacemaker cycle). Inexcitability was evident at critical diastolic intervals where vagal input prevented atrial impulses from activating the pacemaker allowing spontaneous discharges to occur, i.e., escape, late in diastole. Besides inexcitability, incidence and timing of escape impulses were determined by cumulative effects of drive cycle length, vagal stimulus, and subthreshold electrotonic input on intrinsic pacemaker cycle. These data suggest that phasic vagal stimuli may transiently protect atrial ectopic pacemaker foci from conducted sinus impulses by rendering pacemaker and surrounding fibers inexcitable. In the setting of a long sinus (drive) cycle length, phasic vagal activity may result in spontaneous discharges manifest as late atrial premature beats.

You may need the vagus nerve to understand pathophysiology and to treat diseases

2011 ◽  
Vol 122 (7) ◽  
pp. 323-328 ◽  
Author(s):  
Marijke De Couck ◽  
Boris Mravec ◽  
Yori Gidron
Keyword(s):  
Risk Factors ◽  
Vagus Nerve ◽  
Vagal Nerve ◽  
Vagal Activity ◽  
Clinical Effects ◽  
Nerve Activity ◽  
Inflammatory Reactions ◽  
Therapeutic Implications ◽  
The Metabolic Syndrome ◽  
Vagal Nerve Activity

Can different pathophysiological mechanisms and risk factors leading to various diseases be linked with altered transmission of signals by one common pathway? The present article provides evidence for the hypothesis that adequate vagal nerve activity reduces the risk of major diseases, via common basic mechanisms and interim risk factors. These diseases include cardiovascular disease, cancer, Alzheimer's disease and the metabolic syndrome. Three basic mechanisms contribute to such illnesses: local oxidative stress and DNA damage, inflammatory reactions and excessive sympathetic responses, all of which are inhibited by vagal nerve activity. Efferent vagal activity that can be non-invasively measured by HRV (heart rate variability), derived from an ECG, is inversely related to all three basic mechanisms, to various risk factors (e.g. diabetes and dyslipidaemia) and, more broadly, to the diseases as well. Finally, vagal activity is proposed to moderate the effects of risk factors on developing such illnesses. By proposing an integrative neurobiological model of major diseases, identifying people at risk for, and treating patients with, such diseases may be done more efficiently. People with low HRV may be identified and subsequently treated by vagus nerve activation to possibly prevent or treat such illnesses. This proposed disease paradigm may have important preventative and therapeutic implications, whose clinical effects need to be investigated.

Basal vagal nerve activity does not predict susceptibility to dofetilide-induced torsade de pointes in anaesthetized rabbits

2006 ◽  
Vol 40 (6) ◽  
pp. 984
Author(s):  
András Farkas ◽  
Attila S. Farkas ◽  
László Rudas ◽  
István Leprán ◽  
Szabolcs Orosz ◽  
...  
Keyword(s):  
Torsade De Pointes ◽  
Vagal Nerve ◽  
Nerve Activity ◽  
Vagal Nerve Activity

The serotonin receptor mediates changes in autonomic neurotransmission and gastrointestinal transit induced by heat-killed Lactobacillus brevis SBC8803

2015 ◽  
Vol 6 (6) ◽  
pp. 817-822 ◽  
Author(s):  
Y. Horii ◽  
Y. Nakakita ◽  
Y. Misonou ◽  
T. Nakamura ◽  
K. Nagai
Keyword(s):  
Receptor Antagonist ◽  
Serotonin Receptor ◽  
Gastrointestinal Transit ◽  
Lactobacillus Brevis ◽  
Vagal Nerve ◽  
Oral Gavage ◽  
Nerve Activity ◽  
Electrophysiological Studies ◽  
Vagal Nerve Activity ◽  
Gi Transit

Lactobacilli exhibit several health benefits in mammals, including humans. Our previous reports established that heat-killed Lactobacillus brevis SBC8803 (SBC8803) increased both efferent gastric vagal nerve activity and afferent intestinal vagal nerve activity in rats. We speculated that this strain could be useful for the treatment of gastrointestinal (GI) disorders. In this study, we examined the effects of SBC8803 on peristalsis and the activity of the efferent celiac vagal nerve innervating the intestine in rats. First, we examined the effects of intraduodenal (ID) administration of SBC8803 on efferent celiac vagal nerve activity (efferent CVNA) in urethane-anesthetised rats using electrophysiological studies. The effects of intravenous injection of the serotonin 5-HT3 receptor antagonist granisetron on changes in efferent CVNA due to ID administration of SBC8803 were also investigated. Finally, the effects of oral gavage of SBC8803 on GI transit were analysed using the charcoal propulsion method in conscious rats treated with or without granisetron. ID administration of SBC8803 increased efferent CVNA. Pretreatment with granisetron eliminated SBC8803-dependent changes in efferent CVNA. Furthermore, oral gavage of SBC8803 significantly accelerated GI transit, while pretreatment with granisetron inhibited GI transit. Our findings suggested that SBC8803 increased efferent CVNA and GI transit of charcoal meal via 5-HT3 receptors. Moreover, SBC8803 enhanced the activity of efferent vagal nerve innervating the intestine and promoted peristalsis via 5-HT3 receptors.

scholarly journals Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases

2018 ◽  
Vol 35 (1) ◽  
pp. 156-166 ◽  
Author(s):  
Longzhu Liu ◽  
Ming Zhao ◽  
Xiaojiang Yu ◽  
Weijin Zang
Keyword(s):  
Cardiovascular Diseases ◽  
Vagal Nerve ◽  
Nerve Activity ◽  
Pharmacological Modulation ◽  
Vagal Nerve Activity

Recording Vagal Nerve Activity for the Control of an Artificial Heart System

ASAIO Journal ◽  
2003 ◽  
Vol 49 (6) ◽  
pp. 698-700 ◽  
Author(s):  
Tomoyuki Yambe ◽  
Shun-suke Nanka ◽  
Yasuyuki Shiraishi ◽  
Akira Tanaka ◽  
Makoto Yoshizawa ◽  
...  
Keyword(s):  
Artificial Heart ◽  
Vagal Nerve ◽  
Nerve Activity ◽  
Vagal Nerve Activity

scholarly journals Esmolol indirectly stimulates vagal nerve activity in endotoxemic pigs

2018 ◽  
Vol 6 (1) ◽  
Author(s):  
Jerome Aboab ◽  
Louis Mayaud ◽  
Veronique Sebille ◽  
Rodrigo de Oliveira ◽  
Merce Jourdain ◽  
...  
Keyword(s):  
Vagal Nerve ◽  
Nerve Activity ◽  
Vagal Nerve Activity

Low-frequency oscillation of sympathetic nerve activity decreases during development of tilt-induced syncope preceding sympathetic withdrawal and bradycardia

2005 ◽  
Vol 289 (4) ◽  
pp. H1758-H1769 ◽  
Author(s):  
Atsunori Kamiya ◽  
Junichiro Hayano ◽  
Toru Kawada ◽  
Daisaku Michikami ◽  
Kenta Yamamoto ◽  
...  
Keyword(s):  
Heart Rate ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Low Frequency ◽  
Vagal Nerve ◽  
Low Frequency Oscillation ◽  
Nerve Activity ◽  
Neurally Mediated Syncope ◽  
Severe Hypotension ◽  
Vagal Nerve Activity

Sympathetic activation during orthostatic stress is accompanied by a marked increase in low-frequency (LF, ∼0.1-Hz) oscillation of sympathetic nerve activity (SNA) when arterial pressure (AP) is well maintained. However, LF oscillation of SNA during development of orthostatic neurally mediated syncope remains unknown. Ten healthy subjects who developed head-up tilt (HUT)-induced syncope and 10 age-matched nonsyncopal controls were studied. Nonstationary time-dependent changes in calf muscle SNA (MSNA, microneurography), R-R interval, and AP (finger photoplethysmography) variability during a 15-min 60° HUT test were assessed using complex demodulation. In both groups, HUT during the first 5 min increased heart rate, magnitude of MSNA, LF and respiratory high-frequency (HF) amplitudes of MSNA variability, and LF and HF amplitudes of AP variability but decreased HF amplitude of R-R interval variability (index of cardiac vagal nerve activity). In the nonsyncopal group, these changes were sustained throughout HUT. In the syncopal group, systolic AP decreased from 100 to 60 s before onset of syncope; LF amplitude of MSNA variability decreased, whereas magnitude of MSNA and LF amplitude of AP variability remained elevated. From 60 s before onset of syncope, MSNA and heart rate decreased, index of cardiac vagal nerve activity increased, and AP further decreased to the level at syncope. LF oscillation of MSNA variability decreased during development of orthostatic neurally mediated syncope, preceding sympathetic withdrawal, bradycardia, and severe hypotension, to the level at syncope.

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