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Functional selectivity of cardiac preganglionic sympathetic neurones in the rabbit heart

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posted on 17.05.2018, 09:04 by Reshma A. Chauhan, John Coote, Emily Allen, Pott Pongpaopattanakul, Kieran E. Brack, G. Andre Ng
BACKGROUND: Studies have shown regional and functional selectivity of cardiac postganglionic neurones indicating there might exist a similar heterogeneity in spinal segmental preganglionic neurones, which requires further investigation. METHODS: Right and left sympathetic chains were electrically stimulated from T6 to T1 in the innervated isolated rabbit heart preparation (n = 18). Sinus rate, left ventricular pressure, retrograde ventriculo-atrial conduction, monophasic action potential duration, effective refractory period, ventricular fibrillation threshold and electrical restitution were measured. RESULTS: Right sympathetic stimulation had a greater influence on heart rate (T1-T2: right; 59.9 ± 6.0%, left; 41.1 ± 5.6% P < 0.001) and left stimulation had greater effects on left ventricular pressure (T1-T2: right; 20.7 ± 3.2%, left; 40.3 ± 5.4%, P < 0.01) and ventriculo-atrial conduction (T1-T2: right; -6.8 ± 1.1%, left; -15.5 ± 0.2%) at all levels, with greater effects at rostral levels (T1-T3). Left sympathetic stimulation caused shorter monophasic action potentials at the base (T4-T5: right; 119.3 ± 2.7 ms, left; 114.7 ± 2.5 ms. P < 0.05) and apex (T4-T5: right; 118.8 ± 1.2 ms, left; 114.6 ± 2.6 ms. P < 0.05), greater shortening of effective refractory period (T4-T5: right; -3.6 ± 1.3%, left; -7.7 ± 1.8%. P < 0.05), a steeper maximum slope of restitution (T4-T5 base: right; 1.3 ± 0.2, left; 1.8 ± 0.2. P < 0.01. T4-T5 apex: right; 1.0 ± 0.2, left; 1.6 ± 0.3. P < 0.05) and a greater decrease in ventricular fibrillation threshold (T4-T5: right; -22.3 ± 6.8%, left;-39.0 ± 1.7%), with dominant effects at caudal levels (T4-T6). CONCLUSIONS: The preganglionic sympathetic efferent axons show functionally distinct pathways to the heart. The caudal segments (T4-T6) of the left sympathetic chain had a greater potential for arrhythmia generation and hence could pose a target for more focused clinical treatments for impairments in cardiac function.

Funding

Work included in this manuscript has been supported by British Heart Foundation Programme Grant (RG/17/3/32774) and TH Wathes studentship.

History

Citation

International Journal of Cardiology, 2018, 264, pp. 70-78

Author affiliation

/Organisation/COLLEGE OF LIFE SCIENCES/School of Medicine/Department of Cardiovascular Sciences

Version

VoR (Version of Record)

Published in

International Journal of Cardiology

Publisher

Elsevier, International Society for Adult Congenital Heart Disease

issn

0167-5273

eissn

1874-1754

Acceptance date

26/03/2018

Copyright date

2018

Available date

17/05/2018

Publisher version

https://www.sciencedirect.com/science/article/pii/S0167527317366585?via=ihub

Language

en