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...
Main Authors: | , , , , , , , , , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2021-01-01
|
Series: | Cells |
Subjects: | |
Online Access: | https://www.mdpi.com/2073-4409/10/1/60 |
id |
doaj-06909cd94a5747b4b857ac4e6cb6cc74 |
---|---|
record_format |
Article |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Ji Hyeon Ahn Tae-Kyeong Lee Hyun-Jin Tae Bora Kim Hyejin Sim Jae-Chul Lee Dae Won Kim Yoon Sung Kim Myoung Cheol Shin Yoonsoo Park Jun Hwi Cho Joon Ha Park Choong-Hyun Lee Soo Young Choi Moo-Ho Won |
spellingShingle |
Ji Hyeon Ahn Tae-Kyeong Lee Hyun-Jin Tae Bora Kim Hyejin Sim Jae-Chul Lee Dae Won Kim Yoon Sung Kim Myoung Cheol Shin Yoonsoo Park Jun Hwi Cho Joon Ha Park Choong-Hyun Lee Soo Young Choi Moo-Ho Won 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 Cells cardiopulmonary resuscitation Fluoro Jade B prompt hypothermia neuronal death autonomic lower motor neurons myelencephalon |
author_facet |
Ji Hyeon Ahn Tae-Kyeong Lee Hyun-Jin Tae Bora Kim Hyejin Sim Jae-Chul Lee Dae Won Kim Yoon Sung Kim Myoung Cheol Shin Yoonsoo Park Jun Hwi Cho Joon Ha Park Choong-Hyun Lee Soo Young Choi Moo-Ho Won |
author_sort |
Ji Hyeon Ahn |
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_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_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_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 |
publisher |
MDPI AG |
series |
Cells |
issn |
2073-4409 |
publishDate |
2021-01-01 |
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. |
topic |
cardiopulmonary resuscitation Fluoro Jade B prompt hypothermia neuronal death autonomic lower motor neurons myelencephalon |
url |
https://www.mdpi.com/2073-4409/10/1/60 |
work_keys_str_mv |
AT jihyeonahn neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT taekyeonglee neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT hyunjintae neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT borakim neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT hyejinsim neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT jaechullee neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT daewonkim neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT yoonsungkim neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT myoungcheolshin neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT yoonsoopark neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT junhwicho neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT joonhapark neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT choonghyunlee neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT sooyoungchoi neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats AT moohowon neuronaldeathinthecnsautonomiccontrolcentercomesveryearlyaftercardiacarrestandisnotsignificantlyattenuatedbyprompthypothermictreatmentinrats |
_version_ |
1724351188735885312 |
spelling |
doaj-06909cd94a5747b4b857ac4e6cb6cc742021-01-03T00:01:14ZengMDPI AGCells2073-44092021-01-0110606010.3390/cells10010060Neuronal Death in the CNS Autonomic Control Center Comes Very Early after Cardiac Arrest and Is Not Significantly Attenuated by Prompt Hypothermic Treatment in RatsJi Hyeon Ahn0Tae-Kyeong Lee1Hyun-Jin Tae2Bora Kim3Hyejin Sim4Jae-Chul Lee5Dae Won Kim6Yoon Sung Kim7Myoung Cheol Shin8Yoonsoo Park9Jun Hwi Cho10Joon Ha Park11Choong-Hyun Lee12Soo Young Choi13Moo-Ho Won14Department of Physical Therapy, College of Health Science, Youngsan University, Yangsan 50510, KoreaDepartment of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon 24252, KoreaBio-Safety Research Institute, College of Veterinary Medicine, Chonbuk National University, Iksan 54596, KoreaDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 24341, KoreaDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 24341, KoreaDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 24341, KoreaDepartment of Biochemistry and Molecular Biology, and Research Institute of Oral Sciences, College of Dentistry, Gangnung-Wonju National University, Gangneung 25457, KoreaDepartment of Emergency Medicine, Samcheok Medical Center, Samcheok 25920, KoreaDepartment of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon 24341, KoreaDepartment of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon 24341, KoreaDepartment of Emergency Medicine, School of Medicine, Kangwon National University, Chuncheon 24341, KoreaDepartment of Anatomy, College of Korean Medicine, Dongguk University, Gyeongju 38066, KoreaDepartment of Pharmacy, College of Pharmacy, Dankook University, Cheonan 31116, KoreaDepartment of Biomedical Science and Research Institute for Bioscience and Biotechnology, Hallym University, Chuncheon 24252, KoreaDepartment of Neurobiology, School of Medicine, Kangwon National University, Chuncheon 24341, KoreaAutonomic 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.https://www.mdpi.com/2073-4409/10/1/60cardiopulmonary resuscitationFluoro Jade Bprompt hypothermianeuronal deathautonomic lower motor neuronsmyelencephalon |