High-potential defense mechanisms of neocortex in a rat model of transient asphyxia induced cardiac arrest

Keilhoff, Gerburg; Esser, Torben; Titze, Maximilian; Ebmeyer, Uwe; Schild, Lorenz

doi:10.1016/j.brainres.2017.08.018

Cited by 8 publications

(4 citation statements)

References 82 publications

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“…The activation of microglia, reflecting the inflammatory response in the central nervous system, is one of the key processes correlated with ischemic neuronal death because they release cytotoxic and pro-inflammatory cytokines such as interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and reactive oxygen species [33][34][35]. CA was reported to increase activated Iba-1 immunoreactive microglia [2,36], and microglial TNF-α and IL-1β gene expression levels [37] in the rat brain. Consistent with these established studies, in our current study, Iba-1 immunoreactivity was markedly increased in relation to neuronal death in the above-mentioned nuclei or areas and was highest 2 days post-CA.…”

Section: Discussionmentioning

confidence: 99%

“…Cardiac arrest (CA) is mainly caused by lack of oxygen (asphyxia), and ventricular fibrillation and is one of the major causes of death [1]. A large number of patients with CA do not survive long or experience neurological disabilities due to ischemia-reperfusion (IR) injury [2,3]. In particular, airway obstruction, respiratory failure, pulmonary embolism, drowning, and choking are common causes of asphyxial CA [4].…”

Section: Introductionmentioning

confidence: 99%

“…Despite the important role of the myelencephalon in survival and death after brain insults [9], there has been less evidence for the role of neuronal damage and death in the central nervous system (CNS) autonomic control center. Most of the previous studies on ischemic brain damage after asphyxial CA have been conducted in confined areas such as the cerebral cortex, hippocampus and cerebellum using the TUNEL method [2] or morphological analyses using hematoxylin and eosin staining [1,10] and toluidine blue staining [11].…”

Section: Introductionmentioning

confidence: 99%

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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

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%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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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

Ahn

Lee

Tae

et al. 2021

Cells

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“…ROSC was defined as the return of supraventricular rhythm with an increase in MAP >50 mmHg for 5 min. Only rats that achieved ROSC within 10 min were used for further studies (25)(26)(27). This criterion was to avoid non-homogeneous CA periods leading to pathophysiological differences and subsequently to the need for larger numbers of animals.…”

Section: Methodsmentioning

confidence: 99%

Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis

Fan

et al. 2020

Mol Med Rep

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Post-cardiac arrest myocardial dysfunction (PAMD) is a leading cause of death in patients undergoing resuscitation patients following cardiac arrest (CA). Although prostaglandin E1 (PGE1) is a clinical drug used to mitigate ischemia injury, its effect on PAMD remains unknown. In the present study, the protective effects of PGE1 on PAMD were evaluated in a rat model of CA and in a hypoxia-reoxygenation (H/R) in vitro model. Rats were randomly assigned to CA, CA+PGE1 or sham groups. Asphyxia for 8 min followed by cardiopulmonary resuscitation were performed in the CA and CA+PGE1 groups. PGE1 was intravenously administered at the onset of return of spontaneous circulation (ROSC). PGE1 treatment significantly increased the ejection fraction and cardiac output within 4 h following ROSC and improved the survival rate, compared with the CA group. Moreover, PGE1 inactivated GSK3β, prevented mitochondrial permeability transition pore (mPTP) opening, while reducing cytochrome c and cleaved caspase-3 expression, as well as cardiomyocyte apoptosis in the rat model. To examine the underlying mechanism, H/R H9c2 cells were treated with PGE1 at the start of reoxygenation. The changes in GSK3β activity, mPTP opening, cytochrome c and cleaved caspase-3 expression, and apoptosis of H9c2 cells were consistent with those noted in vivo. The results indicated that PGE1 attenuated PAMD by inhibiting mitochondria-mediated cardiomyocyte apoptosis.

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The Neuroprotective Effects of Administration of Methylprednisolone in Cardiopulmonary Resuscitation in Experimental Cardiac Arrest Model

et al. 2022

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High-potential defense mechanisms of neocortex in a rat model of transient asphyxia induced cardiac arrest

Cited by 8 publications

References 82 publications

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

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

Prostaglandin E1 attenuates post‑cardiac arrest myocardial dysfunction through inhibition of mitochondria‑mediated cardiomyocyte apoptosis

The Neuroprotective Effects of Administration of Methylprednisolone in Cardiopulmonary Resuscitation in Experimental Cardiac Arrest Model

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