Cargando…
Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice
BACKGROUND: The aim of this study was to probe cardiac complications, including heart-rate control, in a mouse model of type-2 diabetes. Heart-rate development in diabetic patients is not straight forward: In general, patients with diabetes have faster heart rates compared to non-diabetic individual...
Autores principales: | , , , |
---|---|
Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2014
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4149194/ https://www.ncbi.nlm.nih.gov/pubmed/25113792 http://dx.doi.org/10.1186/s12933-014-0122-y |
_version_ | 1782332714430496768 |
---|---|
author | Soltysinska, Ewa Speerschneider, Tobias Winther, Sine V Thomsen, Morten B |
author_facet | Soltysinska, Ewa Speerschneider, Tobias Winther, Sine V Thomsen, Morten B |
author_sort | Soltysinska, Ewa |
collection | PubMed |
description | BACKGROUND: The aim of this study was to probe cardiac complications, including heart-rate control, in a mouse model of type-2 diabetes. Heart-rate development in diabetic patients is not straight forward: In general, patients with diabetes have faster heart rates compared to non-diabetic individuals, yet diabetic patients are frequently found among patients treated for slow heart rates. Hence, we hypothesized that sinoatrial node (SAN) dysfunction could contribute to our understanding of the mechanism behind this conundrum and the consequences thereof. METHODS: Cardiac hemodynamic and electrophysiological characteristics were investigated in diabetic db/db and control db/+ mice. RESULTS: We found improved contractile function and impaired filling dynamics of the heart in db/db mice, relative to db/+ controls. Electrophysiologically, we observed comparable heart rates in the two mouse groups, but SAN recovery time was prolonged in diabetic mice. Adrenoreceptor stimulation increased heart rate in all mice and elicited cardiac arrhythmias in db/db mice only. The arrhythmias emanated from the SAN and were characterized by large RR fluctuations. Moreover, nerve density was reduced in the SAN region. CONCLUSIONS: Enhanced systolic function and reduced diastolic function indicates early ventricular remodeling in obese and diabetic mice. They have SAN dysfunction, and adrenoreceptor stimulation triggers cardiac arrhythmia originating in the SAN. Thus, dysfunction of the intrinsic cardiac pacemaker and remodeling of the autonomic nervous system may conspire to increase cardiac mortality in diabetic patients. |
format | Online Article Text |
id | pubmed-4149194 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-41491942014-08-30 Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice Soltysinska, Ewa Speerschneider, Tobias Winther, Sine V Thomsen, Morten B Cardiovasc Diabetol Original Investigation BACKGROUND: The aim of this study was to probe cardiac complications, including heart-rate control, in a mouse model of type-2 diabetes. Heart-rate development in diabetic patients is not straight forward: In general, patients with diabetes have faster heart rates compared to non-diabetic individuals, yet diabetic patients are frequently found among patients treated for slow heart rates. Hence, we hypothesized that sinoatrial node (SAN) dysfunction could contribute to our understanding of the mechanism behind this conundrum and the consequences thereof. METHODS: Cardiac hemodynamic and electrophysiological characteristics were investigated in diabetic db/db and control db/+ mice. RESULTS: We found improved contractile function and impaired filling dynamics of the heart in db/db mice, relative to db/+ controls. Electrophysiologically, we observed comparable heart rates in the two mouse groups, but SAN recovery time was prolonged in diabetic mice. Adrenoreceptor stimulation increased heart rate in all mice and elicited cardiac arrhythmias in db/db mice only. The arrhythmias emanated from the SAN and were characterized by large RR fluctuations. Moreover, nerve density was reduced in the SAN region. CONCLUSIONS: Enhanced systolic function and reduced diastolic function indicates early ventricular remodeling in obese and diabetic mice. They have SAN dysfunction, and adrenoreceptor stimulation triggers cardiac arrhythmia originating in the SAN. Thus, dysfunction of the intrinsic cardiac pacemaker and remodeling of the autonomic nervous system may conspire to increase cardiac mortality in diabetic patients. BioMed Central 2014-08-12 /pmc/articles/PMC4149194/ /pubmed/25113792 http://dx.doi.org/10.1186/s12933-014-0122-y Text en © Soltysinska et al.; licensee BioMed Central Ltd. 2014 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Original Investigation Soltysinska, Ewa Speerschneider, Tobias Winther, Sine V Thomsen, Morten B Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice |
title | Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice |
title_full | Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice |
title_fullStr | Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice |
title_full_unstemmed | Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice |
title_short | Sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice |
title_sort | sinoatrial node dysfunction induces cardiac arrhythmias in diabetic mice |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4149194/ https://www.ncbi.nlm.nih.gov/pubmed/25113792 http://dx.doi.org/10.1186/s12933-014-0122-y |
work_keys_str_mv | AT soltysinskaewa sinoatrialnodedysfunctioninducescardiacarrhythmiasindiabeticmice AT speerschneidertobias sinoatrialnodedysfunctioninducescardiacarrhythmiasindiabeticmice AT winthersinev sinoatrialnodedysfunctioninducescardiacarrhythmiasindiabeticmice AT thomsenmortenb sinoatrialnodedysfunctioninducescardiacarrhythmiasindiabeticmice |