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Vagus nerve stimulation-induced bradyarrhythmias in rats.
Auton Neurosci. 2009 Dec 03; 151(2):98-105.AN

Abstract

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.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Hotta H
Department of the Autonomic Nervous System, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
Lazar J
No affiliation info available
Orman R
No affiliation info available
Koizumi K
No affiliation info available
Shiba K
No affiliation info available
Kamran H
No affiliation info available
Stewart M
No affiliation info available

MeSH

AnimalsApneaAutonomic Nervous System DiseasesBlood PressureBradycardiaDeath, Sudden, CardiacDisease Models, AnimalEpilepsyHeartHeart Conduction SystemHeart RateMaleParasympathetic Nervous SystemRatsRats, WistarStroke VolumeSympathetic Nervous SystemVagus NerveVagus Nerve DiseasesVagus Nerve Stimulation

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19651541

Citation

Hotta, Harumi, et al. "Vagus Nerve Stimulation-induced Bradyarrhythmias in Rats." Autonomic Neuroscience : Basic & Clinical, vol. 151, no. 2, 2009, pp. 98-105.
Hotta H, Lazar J, Orman R, et al. Vagus nerve stimulation-induced bradyarrhythmias in rats. Auton Neurosci. 2009;151(2):98-105.
Hotta, H., Lazar, J., Orman, R., Koizumi, K., Shiba, K., Kamran, H., & Stewart, M. (2009). Vagus nerve stimulation-induced bradyarrhythmias in rats. Autonomic Neuroscience : Basic & Clinical, 151(2), 98-105. https://doi.org/10.1016/j.autneu.2009.07.008
Hotta H, et al. Vagus Nerve Stimulation-induced Bradyarrhythmias in Rats. Auton Neurosci. 2009 Dec 3;151(2):98-105. PubMed PMID: 19651541.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vagus nerve stimulation-induced bradyarrhythmias in rats. AU - Hotta,Harumi, AU - Lazar,Jason, AU - Orman,Rena, AU - Koizumi,Kiyomi, AU - Shiba,Kanako, AU - Kamran,Haroon, AU - Stewart,Mark, Y1 - 2009/08/03/ PY - 2009/04/17/received PY - 2009/07/07/revised PY - 2009/07/10/accepted PY - 2009/8/5/entrez PY - 2009/8/5/pubmed PY - 2010/2/2/medline SP - 98 EP - 105 JF - Autonomic neuroscience : basic & clinical JO - Auton Neurosci VL - 151 IS - 2 N2 - 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. SN - 1872-7484 UR - https://www.unboundmedicine.com/medline/citation/19651541/Vagus_nerve_stimulation_induced_bradyarrhythmias_in_rats_ DB - PRIME DP - Unbound Medicine ER -