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Establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia
OBJECTIVE: Cardiac arrest (CA) is caused by a nonshockable rhythm with a low success rate of return of spontaneous circulation (ROSC) and a poor prognosis. This study intended to establish a nonshockable rhythm CA model caused by asphyxia. MATERIALS AND METHODS: Healthy adult male Wistar rats were i...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9798662/ https://www.ncbi.nlm.nih.gov/pubmed/36581829 http://dx.doi.org/10.1186/s12872-022-02996-w |
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author | Zhang, Chenyu Zhan, Haohong Zhou, Dawang Li, Tian Zhang, Qiang Liu, Cong Wei, Hongyan Hu, Chunlin |
author_facet | Zhang, Chenyu Zhan, Haohong Zhou, Dawang Li, Tian Zhang, Qiang Liu, Cong Wei, Hongyan Hu, Chunlin |
author_sort | Zhang, Chenyu |
collection | PubMed |
description | OBJECTIVE: Cardiac arrest (CA) is caused by a nonshockable rhythm with a low success rate of return of spontaneous circulation (ROSC) and a poor prognosis. This study intended to establish a nonshockable rhythm CA model caused by asphyxia. MATERIALS AND METHODS: Healthy adult male Wistar rats were injected with vecuronium bromide to induce CA. After the CA duration reached the target time point, cardiopulmonary resuscitation was performed. The survival status and neurological and cardiac function were evaluated after ROSC. Brain histopathology, including hematoxylin staining, Nissl staining and Terminal dUTP nick-end labeling (TUNEL) staining, was performed to evaluate the surviving cells and apoptotic cells. Apoptosis-related proteins after ROSC for 72 h were analyzed by western blot. RESULTS: CA was successfully induced in all animals. The time for the three groups of animals to PEA was 320 ± 22 s in the CA-8 group, 322 ± 28 s in the CA-12 group and 320 ± 18 s in the CA-15 group. The time to asystole was 436 ± 54 s in the CA-8 group, 438 ± 62 s in the CA-12 group and 433 ± 56 s in the CA-15 group. The NDS of rats in the CA group was significantly decreased after ROSC for 24 h. The NDS in the CA-15 group was 5–16 points, while it was 58–67 points and 15–43 points in the CA-8 and CA-12 groups, respectively. The cardiac function of animals in the CA group was impaired after ROSC, and the ejection fraction, fractional shortening, stroke volume and cardiac output, were all significantly decreased. Brain histopathology showed that the number of surviving neurons was decreased, and the number of apoptotic cells was increased in CA group, the longer the CA duration, the more apoptotic cells increased. The expression of the proapoptotic protein Bax and the apoptotic executive protein caspase3 in the hippocampus of CA rats was significantly increased, while the expression of the antiapoptotic protein Bcl-2 was significantly reduced. CONCLUSIONS: The use of vecuronium can successfully induce CA caused by nonshockable rhythm in rats, which will help to further study the pathophysiological changes after CA by nonshockable rhythm. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12872-022-02996-w. |
format | Online Article Text |
id | pubmed-9798662 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-97986622022-12-30 Establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia Zhang, Chenyu Zhan, Haohong Zhou, Dawang Li, Tian Zhang, Qiang Liu, Cong Wei, Hongyan Hu, Chunlin BMC Cardiovasc Disord Research OBJECTIVE: Cardiac arrest (CA) is caused by a nonshockable rhythm with a low success rate of return of spontaneous circulation (ROSC) and a poor prognosis. This study intended to establish a nonshockable rhythm CA model caused by asphyxia. MATERIALS AND METHODS: Healthy adult male Wistar rats were injected with vecuronium bromide to induce CA. After the CA duration reached the target time point, cardiopulmonary resuscitation was performed. The survival status and neurological and cardiac function were evaluated after ROSC. Brain histopathology, including hematoxylin staining, Nissl staining and Terminal dUTP nick-end labeling (TUNEL) staining, was performed to evaluate the surviving cells and apoptotic cells. Apoptosis-related proteins after ROSC for 72 h were analyzed by western blot. RESULTS: CA was successfully induced in all animals. The time for the three groups of animals to PEA was 320 ± 22 s in the CA-8 group, 322 ± 28 s in the CA-12 group and 320 ± 18 s in the CA-15 group. The time to asystole was 436 ± 54 s in the CA-8 group, 438 ± 62 s in the CA-12 group and 433 ± 56 s in the CA-15 group. The NDS of rats in the CA group was significantly decreased after ROSC for 24 h. The NDS in the CA-15 group was 5–16 points, while it was 58–67 points and 15–43 points in the CA-8 and CA-12 groups, respectively. The cardiac function of animals in the CA group was impaired after ROSC, and the ejection fraction, fractional shortening, stroke volume and cardiac output, were all significantly decreased. Brain histopathology showed that the number of surviving neurons was decreased, and the number of apoptotic cells was increased in CA group, the longer the CA duration, the more apoptotic cells increased. The expression of the proapoptotic protein Bax and the apoptotic executive protein caspase3 in the hippocampus of CA rats was significantly increased, while the expression of the antiapoptotic protein Bcl-2 was significantly reduced. CONCLUSIONS: The use of vecuronium can successfully induce CA caused by nonshockable rhythm in rats, which will help to further study the pathophysiological changes after CA by nonshockable rhythm. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12872-022-02996-w. BioMed Central 2022-12-29 /pmc/articles/PMC9798662/ /pubmed/36581829 http://dx.doi.org/10.1186/s12872-022-02996-w Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) . The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/ (https://creativecommons.org/publicdomain/zero/1.0/) ) applies to the data made available in this article, unless otherwise stated in a credit line to the data. |
spellingShingle | Research Zhang, Chenyu Zhan, Haohong Zhou, Dawang Li, Tian Zhang, Qiang Liu, Cong Wei, Hongyan Hu, Chunlin Establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia |
title | Establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia |
title_full | Establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia |
title_fullStr | Establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia |
title_full_unstemmed | Establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia |
title_short | Establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia |
title_sort | establishment of a nonshockable rhythm cardiac arrest model caused by asphyxia |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9798662/ https://www.ncbi.nlm.nih.gov/pubmed/36581829 http://dx.doi.org/10.1186/s12872-022-02996-w |
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