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Autonomic Dysfunction Determines Stress-Induced Cardiovascular and Immune Complications in Mice
BACKGROUND: Clinical studies suggest that acute inflammation in patients with elevated heart rate (HR) increases morbidity and mortality. The SJL/J (SJL) inbred mouse strain is a unique genetic model that has higher HR and systemic and vascular inflammation compared with C3HeB/FeJ (C3HeB) mice. The...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley & Sons, Ltd
2015
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599426/ https://www.ncbi.nlm.nih.gov/pubmed/25999402 http://dx.doi.org/10.1161/JAHA.115.001952 |
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author | Batchu, Sri N Smolock, Elaine M Dyachenko, Igor A Murashev, Arkady N Korshunov, Vyacheslav A |
author_facet | Batchu, Sri N Smolock, Elaine M Dyachenko, Igor A Murashev, Arkady N Korshunov, Vyacheslav A |
author_sort | Batchu, Sri N |
collection | PubMed |
description | BACKGROUND: Clinical studies suggest that acute inflammation in patients with elevated heart rate (HR) increases morbidity and mortality. The SJL/J (SJL) inbred mouse strain is a unique genetic model that has higher HR and systemic and vascular inflammation compared with C3HeB/FeJ (C3HeB) mice. The goal of this study was to investigate the role of stress on cardiac and vascular complications between 2 strains. METHODS AND RESULTS: Radiotelemetry was used for continuous recordings of HR and blood pressure in mice. Hemodynamic differences between mouse strains were very small without stress; however, tail-cuff training generated mild stress and significantly increased HR (≈2-fold) in SJL compared with C3HeB mice. Circulating proinflammatory monocytes (CD11b(+)Ly6C(H)(i)) significantly increased in SJL mice but not in C3HeB mice after stress. Presence of Ly6C(+) cells in injured carotids was elevated only in SJL mice after stress; however, a transfer of bone marrow cells from SJL/C3HeB to C3HeB/SJL chimeras had no effect on HR or vascular inflammation following stress. Arterial inflammation (VCAM-1(+)) was greater in SJL inbred mice or SJL recipient chimeras, even without stress or injury. HR variability was reduced in SJL mice compared with C3HeB mice. CONCLUSIONS: We found that impaired parasympathetic activity is central for stress-induced elevation of HR and systemic and vascular inflammation; however, immune cells from stress-susceptible mice had no effect on HR or vascular inflammation in stress-protected mice. |
format | Online Article Text |
id | pubmed-4599426 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2015 |
publisher | John Wiley & Sons, Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-45994262015-10-16 Autonomic Dysfunction Determines Stress-Induced Cardiovascular and Immune Complications in Mice Batchu, Sri N Smolock, Elaine M Dyachenko, Igor A Murashev, Arkady N Korshunov, Vyacheslav A J Am Heart Assoc Original Research BACKGROUND: Clinical studies suggest that acute inflammation in patients with elevated heart rate (HR) increases morbidity and mortality. The SJL/J (SJL) inbred mouse strain is a unique genetic model that has higher HR and systemic and vascular inflammation compared with C3HeB/FeJ (C3HeB) mice. The goal of this study was to investigate the role of stress on cardiac and vascular complications between 2 strains. METHODS AND RESULTS: Radiotelemetry was used for continuous recordings of HR and blood pressure in mice. Hemodynamic differences between mouse strains were very small without stress; however, tail-cuff training generated mild stress and significantly increased HR (≈2-fold) in SJL compared with C3HeB mice. Circulating proinflammatory monocytes (CD11b(+)Ly6C(H)(i)) significantly increased in SJL mice but not in C3HeB mice after stress. Presence of Ly6C(+) cells in injured carotids was elevated only in SJL mice after stress; however, a transfer of bone marrow cells from SJL/C3HeB to C3HeB/SJL chimeras had no effect on HR or vascular inflammation following stress. Arterial inflammation (VCAM-1(+)) was greater in SJL inbred mice or SJL recipient chimeras, even without stress or injury. HR variability was reduced in SJL mice compared with C3HeB mice. CONCLUSIONS: We found that impaired parasympathetic activity is central for stress-induced elevation of HR and systemic and vascular inflammation; however, immune cells from stress-susceptible mice had no effect on HR or vascular inflammation in stress-protected mice. John Wiley & Sons, Ltd 2015-05-21 /pmc/articles/PMC4599426/ /pubmed/25999402 http://dx.doi.org/10.1161/JAHA.115.001952 Text en © 2015 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley Blackwell. http://creativecommons.org/licenses/by-nc/4.0/ This is an open access article under the terms of the Creative Commons Attribution-NonCommercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. |
spellingShingle | Original Research Batchu, Sri N Smolock, Elaine M Dyachenko, Igor A Murashev, Arkady N Korshunov, Vyacheslav A Autonomic Dysfunction Determines Stress-Induced Cardiovascular and Immune Complications in Mice |
title | Autonomic Dysfunction Determines Stress-Induced Cardiovascular and Immune Complications in Mice |
title_full | Autonomic Dysfunction Determines Stress-Induced Cardiovascular and Immune Complications in Mice |
title_fullStr | Autonomic Dysfunction Determines Stress-Induced Cardiovascular and Immune Complications in Mice |
title_full_unstemmed | Autonomic Dysfunction Determines Stress-Induced Cardiovascular and Immune Complications in Mice |
title_short | Autonomic Dysfunction Determines Stress-Induced Cardiovascular and Immune Complications in Mice |
title_sort | autonomic dysfunction determines stress-induced cardiovascular and immune complications in mice |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4599426/ https://www.ncbi.nlm.nih.gov/pubmed/25999402 http://dx.doi.org/10.1161/JAHA.115.001952 |
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