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Published in: Clinical Autonomic Research 3/2018

01-06-2018 | Research Article

Sympathetic mechanisms in an animal model of vasovagal syncope

Authors: Wenbo He, Xiaoying Wang, Shan Liu, Xiaomei Yu, Zhibing Lu, Ruisong Ma, Da Luo, Jing Xie, Bo He, Hong Jiang

Published in: Clinical Autonomic Research | Issue 3/2018

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Abstract

Purpose

Individuals predisposed to vasovagal syncope may have different autonomic nervous system control mechanisms from those without predisposition to vasovagal events. To test this hypothesis, we investigated different sympathetic responses in a canine model of vasovagal syncope.

Methods

Left thoracotomy was performed on 20 mongrel dogs. The heart was exposed and a bolus of veratridine (15 μg/kg), a neurotoxin which prevents the inactivation of sodium ion channels, was injected into the left atrium to induce a Bezold–Jarisch reflex-mediated vasovagal event, characterized by bradycardia, decreased inotropism, and hypotension. Electrocardiogram and blood pressure were continuously monitored. Neural activity was recorded from the left stellate ganglion. Plasma norepinephrine and acetylcholine levels were measured 30 s before and 30 s after veratridine injection.

Results

Veratridine resulted in rapid decreases in heart rate and blood pressure in all dogs, accompanied by increases in both norepinephrine and acetylcholine. Two types of neural activity (high-amplitude spike discharge activity and low-amplitude burst discharge activity) were recorded from the left stellate ganglion. Veratridine induced high-frequency spike discharge activity in some dogs (Group A), whereas spike discharge activity was scarce and relatively unresponsive to veratridine in the remaining dogs (Group B). Dogs in Group A had higher plasma norepinephrine levels (111.63 ± 15.1 vs. 48.11 ± 33.81 ng/l, p = 0.002) and less intense drops in heart rate (− 37 ± 24 vs. − 84 ± 28 bpm, p = 0.001) and blood pressure (systolic blood pressure, − 18 ± 15 vs. − 37 ± 13 mmHg, p = 0.009; diastolic blood pressure, − 26 ± 13 vs. − 45 ± 13 mmHg, p = 0.005) compared to dogs in Group B. Similarly, heart rate post-veratridine was higher (102 ± 23 vs. 69 ± 22 bpm, p = 0.004), the veratridine-induced longest RR interval was shorter (0.7 [0.5–0.8] vs. 1.2 [1.1–3.5] s, p < 0.001) and the diastolic and mean arterial pressures post-veratridine were higher (all p < 0.05) in dogs in Group A compared to those in Group B.

Conclusions

Distinct sympathetic activation as represented by left stellate ganglion high-frequency spike discharge activity protected against bradycardia and hypotension in a canine model of vasovagal syncope. Our findings may have therapeutic implications.
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Metadata
Title
Sympathetic mechanisms in an animal model of vasovagal syncope
Authors
Wenbo He
Xiaoying Wang
Shan Liu
Xiaomei Yu
Zhibing Lu
Ruisong Ma
Da Luo
Jing Xie
Bo He
Hong Jiang
Publication date
01-06-2018
Publisher
Springer Berlin Heidelberg
Published in
Clinical Autonomic Research / Issue 3/2018
Print ISSN: 0959-9851
Electronic ISSN: 1619-1560
DOI
https://doi.org/10.1007/s10286-018-0503-5

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