The Spinal Cord Damage in a Rat Asphyxial Cardiac Arrest/Resuscitation Model

Keilhoff, Gerburg; Titze, Maximilian; Rathert, Henning; Thi, Tue Minh Nguyen; Ebmeyer, Uwe

doi:10.1007/s12028-020-01094-z

Cited by 1 publication

(1 citation statement)

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“…In this study, the survival rate of the rats with CA dropped to less than 50% at 1 day, was about 18% at 2 days, and 0% at 5 days after asphyxial CA for 7-8 min. Jia et al (2006) reported a mean survival of 66.9 h (around 2.7 days) after 7 min of asphyxial CA in Wistar rats [20], and halothane ) as an anesthetic and vecuronium (1 mg/kg) in a Wistar rat model of asphyxial CA for 6 min [22]. The difference in mortality rates may be due to the different experimental methods, such as the duration of CA, the types of animal model of CA, body temperature after CA, and the types of anesthetic used.…”

Section: Discussionmentioning

confidence: 99%

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

Lee

Tae

et al. 2021

Cells

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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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Section: Discussionmentioning

confidence: 99%