Document Detail


Vagus nerve stimulation-induced bradyarrhythmias in rats.
MedLine Citation:
PMID:  19651541     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The autonomic consequences of seizures can be severe. Death can follow from autonomic overactivity that causes a parasympathetically mediated bradyarrhythmia. We studied the cardiovascular consequences of unilateral and bilateral stimulation of the distal segments of transected vagus nerve in rats anesthetized with urethane. The range of stimulation rates tested is comparable to the firing rates observed in vagus nerve during seizures. There was a consistent inverse relation between stimulus rate and heart rate with nodal block appearing at 5-10 Hz and minimum HR levels (cardiac standstill) occurring at 50 Hz. Cardiac standstill could last many seconds. Blood pressure during VNS was maintained during lower frequency VNS, but collapsed at frequencies > or =20 Hz to dramatically impair ventricular filling. Recovery of heart rate and blood pressure after VNS was rapid. In the presence of sympathetic co-activation (pharmacological or hypercapnia and/or hypoxia), mean arterial pressure was better maintained and there was much better ventricular filling, but cardiac performance was worse (e.g. ejection fraction derived from echocardiography). The combination of sympathetic and parasympathetic overactivity was sometimes associated with prolonged (> or =20 s) apneic periods during VNS. We conclude that an abrupt increase in parasympathetic activity on the order of 5 times the background of parasympathetic tone can produce transient bradyarrhythmias, and increases on the order of 20 times can produce cardiac standstill, sometimes accompanied by apnea. Our findings suggest that parasympathetically mediated bradyarrhythmia must be accompanied by airway obstruction to sustain parasympathetic overactivity and produce hypoxia to ultimately cause death.
Authors:
Harumi Hotta; Jason Lazar; Rena Orman; Kiyomi Koizumi; Kanako Shiba; Haroon Kamran; Mark Stewart
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-08-03
Journal Detail:
Title:  Autonomic neuroscience : basic & clinical     Volume:  151     ISSN:  1872-7484     ISO Abbreviation:  Auton Neurosci     Publication Date:  2009 Dec 
Date Detail:
Created Date:  2009-11-03     Completed Date:  2010-02-01     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100909359     Medline TA:  Auton Neurosci     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  98-105     Citation Subset:  IM    
Affiliation:
Department of the Autonomic Nervous System, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apnea / etiology,  physiopathology
Autonomic Nervous System Diseases / etiology,  physiopathology*
Blood Pressure / physiology
Bradycardia / etiology,  physiopathology*
Death, Sudden, Cardiac / etiology
Disease Models, Animal
Epilepsy / complications,  physiopathology*
Heart / innervation,  physiopathology
Heart Conduction System / physiopathology
Heart Rate / physiology
Male
Parasympathetic Nervous System / physiopathology*
Rats
Rats, Wistar
Stroke Volume / physiology
Sympathetic Nervous System / physiopathology
Vagus Nerve / physiopathology
Vagus Nerve Diseases / etiology,  physiopathology*
Vagus Nerve Stimulation / adverse effects

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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