Abstract
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.
Highlights
Cardiac arrest (CA) is mainly caused by lack of oxygen, and ventricular fibrillation and is one of the major causes of death [1]
cardiac arrest (CA), we investigated the effects regions in the central nervous system (CNS) correlate with death following CA, we investigated the effects of hyof hypothermia the mortality rate, neuronal damage/death and microgliosis after pothermia on theon mortality rate, neuronal damage/death and microgliosis after asphyxial asphyxial CA
To investigate the factors affecting of the survival rate after CA, we examined the vulnerable areas in various brain regions related to autonomic function including the cingulate cortex, hippocampus, thalamus, hypothalamus, amygdala, myelencephalon, and the spinal cord after CA using Fluoro-Jade B (F-JB) fluorescence staining
Summary
Cardiac arrest (CA) is mainly caused by lack of oxygen (asphyxia), and ventricular fibrillation and is one of the major causes of death [1]. To find potential therapeutic targets for neuroprotection and increase the survival rate after CA, it is important to investigate when and where neuronal damage and death occurs in the central nervous system (brain and spinal cord). We examined the prevalence of neuronal damage/death in important brain regions (including in the cortex, striatum, thalamus, hypothalamus, hippocampus, substantia nigra, and myelencephalon) and spinal cord using Fluoro-Jade B (F-JB), which is an excellent marker for neuronal degeneration and death [12,13]. We investigated the relationship between neuronal damage and death and the mortality rate of rats after asphyxial CA, and estimated survival rate from applying prompt hypothermic therapy after CA
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