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Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats
Autonomic dysfunction in the central nervous system (CNS) can cause death after recovery from a cardiac arrest (CA). However, few studies on histopathological changes in animal models of CA have been reported. In this study, we investigated the prevalence of neuronal death and damage in various brai...
Autores principales: | , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7824613/ https://www.ncbi.nlm.nih.gov/pubmed/33401719 http://dx.doi.org/10.3390/cells10010060 |
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author | Ahn, Ji Hyeon Lee, Tae-Kyeong Tae, Hyun-Jin Kim, Bora Sim, Hyejin Lee, Jae-Chul Kim, Dae Won Kim, Yoon Sung Shin, Myoung Cheol Park, Yoonsoo Cho, Jun Hwi Park, Joon Ha Lee, Choong-Hyun Choi, Soo Young Won, Moo-Ho |
author_facet | Ahn, Ji Hyeon Lee, Tae-Kyeong Tae, Hyun-Jin Kim, Bora Sim, Hyejin Lee, Jae-Chul Kim, Dae Won Kim, Yoon Sung Shin, Myoung Cheol Park, Yoonsoo Cho, Jun Hwi Park, Joon Ha Lee, Choong-Hyun Choi, Soo Young Won, Moo-Ho |
author_sort | Ahn, Ji Hyeon |
collection | PubMed |
description | Autonomic dysfunction in the central nervous system (CNS) can cause death after recovery from a cardiac arrest (CA). However, few studies on histopathological changes in animal models of CA have been reported. In this study, we investigated the prevalence of neuronal death and damage in various brain regions and the spinal cord at early times after asphyxial CA and we studied the relationship between the mortality rate and neuronal damage following hypothermic treatment after CA. Rats were subjected to 7–8 min of asphyxial CA, followed by resuscitation and prompt hypothermic treatment. Eight regions related to autonomic control (the cingulate cortex, hippocampus, thalamus, hypothalamus, myelencephalon, and spinal cord) were examined using cresyl violet (a marker for Nissl substance) and Fluoro-Jade B (a marker for neuronal death). The survival rate was 44.5% 1 day post-CA, 18.2% 2 days post-CA and 0% 5 days post-CA. Neuronal death started 12 h post-CA in the gigantocellular reticular nucleus and caudoventrolateral reticular nucleus in the myelencephalon and lamina VII in the cervical, thoracic, lumbar, and sacral spinal cord, of which neurons are related to autonomic lower motor neurons. In these regions, Iba-1 immunoreactivity indicating microglial activation (microgliosis) was gradually increased with time after CA. Prompt hypothermic treatment increased the survival rate at 5 days after CA with an attenuation of neuronal damages and death in the damaged regions. However, the survival rate was 0% at 12 days after CA. Taken together, our study suggests that the early damage and death of neurons related to autonomic lower motor neurons was significantly related to the high mortality rate after CA and that prompt hypothermic therapy could increase the survival rate temporarily after CA, but could not ultimately save the animal. |
format | Online Article Text |
id | pubmed-7824613 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-78246132021-01-24 Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats Ahn, Ji Hyeon Lee, Tae-Kyeong Tae, Hyun-Jin Kim, Bora Sim, Hyejin Lee, Jae-Chul Kim, Dae Won Kim, Yoon Sung Shin, Myoung Cheol Park, Yoonsoo Cho, Jun Hwi Park, Joon Ha Lee, Choong-Hyun Choi, Soo Young Won, Moo-Ho Cells Article Autonomic dysfunction in the central nervous system (CNS) can cause death after recovery from a cardiac arrest (CA). However, few studies on histopathological changes in animal models of CA have been reported. In this study, we investigated the prevalence of neuronal death and damage in various brain regions and the spinal cord at early times after asphyxial CA and we studied the relationship between the mortality rate and neuronal damage following hypothermic treatment after CA. Rats were subjected to 7–8 min of asphyxial CA, followed by resuscitation and prompt hypothermic treatment. Eight regions related to autonomic control (the cingulate cortex, hippocampus, thalamus, hypothalamus, myelencephalon, and spinal cord) were examined using cresyl violet (a marker for Nissl substance) and Fluoro-Jade B (a marker for neuronal death). The survival rate was 44.5% 1 day post-CA, 18.2% 2 days post-CA and 0% 5 days post-CA. Neuronal death started 12 h post-CA in the gigantocellular reticular nucleus and caudoventrolateral reticular nucleus in the myelencephalon and lamina VII in the cervical, thoracic, lumbar, and sacral spinal cord, of which neurons are related to autonomic lower motor neurons. In these regions, Iba-1 immunoreactivity indicating microglial activation (microgliosis) was gradually increased with time after CA. Prompt hypothermic treatment increased the survival rate at 5 days after CA with an attenuation of neuronal damages and death in the damaged regions. However, the survival rate was 0% at 12 days after CA. Taken together, our study suggests that the early damage and death of neurons related to autonomic lower motor neurons was significantly related to the high mortality rate after CA and that prompt hypothermic therapy could increase the survival rate temporarily after CA, but could not ultimately save the animal. MDPI 2021-01-02 /pmc/articles/PMC7824613/ /pubmed/33401719 http://dx.doi.org/10.3390/cells10010060 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Ahn, Ji Hyeon Lee, Tae-Kyeong Tae, Hyun-Jin Kim, Bora Sim, Hyejin Lee, Jae-Chul Kim, Dae Won Kim, Yoon Sung Shin, Myoung Cheol Park, Yoonsoo Cho, Jun Hwi Park, Joon Ha Lee, Choong-Hyun Choi, Soo Young Won, Moo-Ho Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats |
title | Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats |
title_full | Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats |
title_fullStr | Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats |
title_full_unstemmed | Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats |
title_short | Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in Rats |
title_sort | neuronal death in the cns autonomic control center comes very early after cardiac arrest and is not significantly attenuated by prompt hypothermic treatment in rats |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7824613/ https://www.ncbi.nlm.nih.gov/pubmed/33401719 http://dx.doi.org/10.3390/cells10010060 |
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