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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...

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Autores principales: 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
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
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.
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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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