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Biphasic changes in spontaneous cardiovagal baroreflex sensitivity during passive hyperthermia

Successful adaptation to passive hyperthermia requires continual adjustment of circulation, which is mediated mainly by the autonomic nervous system. The goal of this study was to explore the alterations in spontaneous cardiovagal baroreflex sensitivity (BRS) during exposure to a hot environment. To...

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Autores principales: Turcani, Marian, Ghadhanfar, Elham
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6385277/
https://www.ncbi.nlm.nih.gov/pubmed/30796280
http://dx.doi.org/10.1038/s41598-019-39172-8
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author Turcani, Marian
Ghadhanfar, Elham
author_facet Turcani, Marian
Ghadhanfar, Elham
author_sort Turcani, Marian
collection PubMed
description Successful adaptation to passive hyperthermia requires continual adjustment of circulation, which is mediated mainly by the autonomic nervous system. The goal of this study was to explore the alterations in spontaneous cardiovagal baroreflex sensitivity (BRS) during exposure to a hot environment. To continuously follow changes in core body temperature (Tc), haemodynamics, and BRS, male Wistar-Kyoto rats were implanted with telemetric transmitters. BRS at an ambient temperature of 23 °C was not steady but oscillated with a maximum power in the range of 0.02–0.2 Hz. Exposure to hot air immediately shifted the distribution of BRS to higher values, although Tc remained unchanged (37.2 (0.3) °C), and the average BRS changed from 1.3 (0.3) to 3 (1.4) ms.mmHg(−1), p < 0.0001. The degree of initial cardiovagal baroreflex sensitization explained 57% of the variability in the time to the onset of arterial pressure decline (p = 0.0114). With an increasing Tc (>38.8 (0.6) °C), BRS non-linearly declined, but haemodynamic parameters remained stable even above a Tc of 42 °C when the cardiovagal baroreflex was virtually non-operative. Abrupt full desensitization of the cardiovagal baroreflex with a muscarinic blocker did not induce arterial pressure decline. Our data indicate that a progressive decrease in BRS during passive hyperthermia does not induce haemodynamic instability. The positive association between initial cardiovagal baroreflex sensitization and the time to the onset of arterial pressure decline may reflect the potential protective role of parasympathetic activation during exposure to a hot environment.
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spelling pubmed-63852772019-02-26 Biphasic changes in spontaneous cardiovagal baroreflex sensitivity during passive hyperthermia Turcani, Marian Ghadhanfar, Elham Sci Rep Article Successful adaptation to passive hyperthermia requires continual adjustment of circulation, which is mediated mainly by the autonomic nervous system. The goal of this study was to explore the alterations in spontaneous cardiovagal baroreflex sensitivity (BRS) during exposure to a hot environment. To continuously follow changes in core body temperature (Tc), haemodynamics, and BRS, male Wistar-Kyoto rats were implanted with telemetric transmitters. BRS at an ambient temperature of 23 °C was not steady but oscillated with a maximum power in the range of 0.02–0.2 Hz. Exposure to hot air immediately shifted the distribution of BRS to higher values, although Tc remained unchanged (37.2 (0.3) °C), and the average BRS changed from 1.3 (0.3) to 3 (1.4) ms.mmHg(−1), p < 0.0001. The degree of initial cardiovagal baroreflex sensitization explained 57% of the variability in the time to the onset of arterial pressure decline (p = 0.0114). With an increasing Tc (>38.8 (0.6) °C), BRS non-linearly declined, but haemodynamic parameters remained stable even above a Tc of 42 °C when the cardiovagal baroreflex was virtually non-operative. Abrupt full desensitization of the cardiovagal baroreflex with a muscarinic blocker did not induce arterial pressure decline. Our data indicate that a progressive decrease in BRS during passive hyperthermia does not induce haemodynamic instability. The positive association between initial cardiovagal baroreflex sensitization and the time to the onset of arterial pressure decline may reflect the potential protective role of parasympathetic activation during exposure to a hot environment. Nature Publishing Group UK 2019-02-22 /pmc/articles/PMC6385277/ /pubmed/30796280 http://dx.doi.org/10.1038/s41598-019-39172-8 Text en © The Author(s) 2019 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Turcani, Marian
Ghadhanfar, Elham
Biphasic changes in spontaneous cardiovagal baroreflex sensitivity during passive hyperthermia
title Biphasic changes in spontaneous cardiovagal baroreflex sensitivity during passive hyperthermia
title_full Biphasic changes in spontaneous cardiovagal baroreflex sensitivity during passive hyperthermia
title_fullStr Biphasic changes in spontaneous cardiovagal baroreflex sensitivity during passive hyperthermia
title_full_unstemmed Biphasic changes in spontaneous cardiovagal baroreflex sensitivity during passive hyperthermia
title_short Biphasic changes in spontaneous cardiovagal baroreflex sensitivity during passive hyperthermia
title_sort biphasic changes in spontaneous cardiovagal baroreflex sensitivity during passive hyperthermia
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6385277/
https://www.ncbi.nlm.nih.gov/pubmed/30796280
http://dx.doi.org/10.1038/s41598-019-39172-8
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