scholarly journals 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 ◽  
2021 ◽  
Vol 10 (1) ◽  
pp. 60
Author(s):  
Ji Hyeon Ahn ◽  
Tae-Kyeong Lee ◽  
Hyun-Jin Tae ◽  
Bora Kim ◽  
Hyejin Sim ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cardiac Arrest ◽  
Survival Rate ◽  
Mortality Rate ◽  
Motor Neurons ◽  
Neuronal Death ◽  
Neuronal Damage ◽  
Autonomic Control ◽  
Reticular Nucleus ◽  
Fluoro Jade B

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.

scholarly journals Selective Loss and Selective Sparing of Neurons in the Thalamic Reticular Nucleus following Human Cardiac Arrest

1993 ◽  
Vol 13 (4) ◽  
pp. 558-567 ◽  
Author(s):  
Douglas T. Ross ◽  
David I. Graham
Keyword(s):  
Cardiac Arrest ◽  
Heart Surgery ◽  
Neuronal Damage ◽  
Open Heart Surgery ◽  
Thalamic Reticular Nucleus ◽  
Global Cerebral Ischemia ◽  
Reticular Nucleus ◽  
Thalamic Nuclei ◽  
Attentional Processing ◽  
Thalamic Relay Nuclei

Neurons in the portion of the human thalamic reticular nucleus (RT) associated with the prefrontal cortex and mediodorsal thalamic nuclei were found to be selectively vulnerable to ischemic neuronal damage following relatively short (≤5-min) duration cardiac arrest. In contrast, selective sparing of these RT neurons occurred in cases with longer (>10-min) duration of arrest that was sufficient to produce extensive ischemic neuronal damage throughout the cerebral cortex and thalamic relay nuclei. The selective degeneration of RT neurons appears to require the sustained activity of corticothalamic or thalamocortical projections to the RT following the ischemic insult. Loss of RT neurons associated with the frontal cortex and mediodorsal thalamus may be the biological basis of some types of persisting cognitive deficits in attentional processing experienced by patients following cardiac arrest, open heart surgery, or other forms of brief global cerebral ischemia.

Abstract WP260: Pravastatin Improves Short-term Survival Rate Following Cardiac Arrest and Cardiopulumonary Resuscitation In Mice

Stroke ◽  
2013 ◽  
Vol 44 (suppl_1) ◽  
Author(s):  
Shin Nakayama ◽  
Noriko Taguchi ◽  
Makoto Tanaka
Keyword(s):  
Body Weight ◽  
Cardiac Arrest ◽  
Survival Rate ◽  
Neuronal Damage ◽  
Pleiotropic Effects ◽  
Histological Evaluation ◽  
Vehicle Group ◽  
Short Term ◽  
Term Survival ◽  
Short Term Survival

Statins (HMG-CoA reductase inhibitors) exert numerous pleiotropic effects and have been shown to attenuate ischemic injury in different rodent models of cerebral focal ischemia. Few studies have examined the effect of statins on post cardiac arrest syndrome. This study conducted cardiac arrest and cardiopulmonary resuscitation (CA/CPR) in mice and tested the hypothesis that intravenous statin after CPR improves survival rate and neurological outcomes. Methods: Adult male mice (20-26 g) were subjected to CA induced by intravenous (IV) KCL. After 8 min of CA, CPR was initiated with IV epinephrine, ventilation with 100% oxygen and chest compressions (rate 300/min). At 1 hr after return of spontaneous circulation, mice were treated with either IV injection of pravastatin (3mg/kg) or vehicle. Four days after CA/CPR, neurobehavioral assessments were performed and brains were removed for histological evaluation in hippocampus and caudateputamen. Results: No difference was found between two groups in body weight, duration of CPR and dose of epinephrine. Survival rate at 4 days after CPR was significantly higher in pravastatin group compared with vehicle group (66.7%; n=24 vs 48.4%; n=33). Neurobehavioral scores in pravastatin group were better than vehicle group at 2 to 4 days after CPR. Body weight loss in vehicle group at 4 days after CPR was higher than pravastatin group (-19.4±1.8% vs -13.4±2.0%), which indicates loss of feeding activity. Histological damages in hippocampus and caudateputamen were not statistically different between two groups (pravastatin: 23.8±7.0% vs vehicle: 35.2±9.2% in hippocampus) (pravastatin: 49.4±7.2% vs vehicle: 60.5±7.8% in caudateputamen). All values are presented as mean±SEM. Conclusions: Single IV injection of pravastatin after CA improved short-term survival and neurobehavioral score in the mouse experimental CA model. Neuronal damage in the brain region was comparable to vehicle group. These data suggest that pravastatin given after CA would be beneficial in the post resuscitation phase via systemic pleiotropic effects such as anti inflammatory response and improved vascular reactivity.

Neuronal damage in rat brain and spinal cord after cardiac arrest and massive hemorrhagic shock*

2006 ◽  
Vol 34 (11) ◽  
pp. 2820-2826 ◽  
Author(s):  
Yoshifumi Kudo ◽  
Hirokazu Ohtaki ◽  
Kenji Dohi ◽  
Li Yin ◽  
Tomoya Nakamachi ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Cardiac Arrest ◽  
Hemorrhagic Shock ◽  
Rat Brain ◽  
Neuronal Damage ◽  
Brain And Spinal Cord

scholarly journals Therapeutic Effects of Risperidone against Spinal Cord Injury in a Rat Model of Asphyxial Cardiac Arrest: A Focus on Body Temperature, Paraplegia, Motor Neuron Damage, and Neuroinflammation

2021 ◽  
Vol 8 (10) ◽  
pp. 230
Author(s):  
Tae-Kyeong Lee ◽  
Jae-Chul Lee ◽  
Hyun-Jin Tae ◽  
Hyung-Il Kim ◽  
Myoung Cheol Shin ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Cardiac Arrest ◽  
Inflammatory Cytokines ◽  
Motor Neurons ◽  
Anterior Horn ◽  
Motor Deficits ◽  
Cord Injury ◽  
Anti Inflammatory ◽  
Pro Inflammatory Cytokines

Cardiac arrest (CA) causes severe spinal cord injury and evokes spinal cord disorders including paraplegia. It has been reported that risperidone, an antipsychotic drug, effectively protects neuronal cell death from transient ischemia injury in gerbil brains. However, until now, studies on the effects of risperidone on spinal cord injury after asphyxial CA (ACA) and cardiopulmonary resuscitation (CPR) are not sufficient. Therefore, this study investigated the effect of risperidone on hind limb motor deficits and neuronal damage/death in the lumbar part of the spinal cord following ACA in rats. Mortality, severe motor deficits in the hind limbs, and the damage/death (loss) of motor neurons located in the anterior horn were observed two days after ACA/CPR. These symptoms were significantly alleviated by risperidone (an atypical antipsychotic) treatment after ACA. In vehicle-treated rats, the immunoreactivities of tumor necrosis factor-alpha (TNF-α) and interleukin 1-beta (IL-1β), as pro-inflammatory cytokines, were increased, and the immunoreactivities of IL-4 and IL-13, as anti-inflammatory cytokines, were reduced with time after ACA/CPR. In contrast, in risperidone-treated rats, the immunoreactivity of the pro-inflammatory cytokines was significantly decreased, and the anti-inflammatory cytokines were enhanced compared to vehicle-treated rats. In brief, risperidone treatment after ACA/CPR in rats significantly improved the survival rate and attenuated paralysis, the damage/death (loss) of motor neurons, and inflammation in the lumbar anterior horn. Thus, risperidone might be a therapeutic agent for paraplegia by attenuation of the damage/death (loss) of spinal motor neurons and neuroinflammation after ACA/CPR.

scholarly journals Minocycline Reduces Neuronal Death and Attenuates Microglial Response after Pediatric Asphyxial Cardiac Arrest

2009 ◽  
Vol 30 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Minke Tang ◽  
Henry Alexander ◽  
Robert SB Clark ◽  
Patrick M Kochanek ◽  
Valerian E Kagan ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Neuronal Death ◽  
Calcium Binding ◽  
Microglial Activation ◽  
Neuronal Degeneration ◽  
Spontaneous Circulation ◽  
Developing Brain ◽  
Fluoro Jade B ◽  
Microglial Response ◽  
Asphyxial Cardiac Arrest

The mechanisms leading to delayed neuronal death after asphyxial cardiac arrest (ACA) in the developing brain are unknown. This study aimed at investigating the possible role of microglial activation in neuronal death in developing brain after ACA. Postnatal day-17 rats were subjected to 9 mins of ACA followed by resuscitation. Rats were randomized to treatment with minocycline, (90 mg/kg, intraperitoneally (i.p.)) or vehicle (saline, i.p.) at 1 h after return of spontaneous circulation. Thereafter, minocycline (22.5 mg/kg, i.p.) was administrated every 12 h until sacrifice. Microglial activation (evaluated by immunohistochemistry using ionized calcium-binding adapter molecule-1 (Iba1) antibody) coincided with DNA fragmentation and neurodegeneration in CA1 hippocampus and cortex (assessed by deoxynucleotidyltransferase-mediated dUTP nick-end labeling (TUNEL), Fluoro-Jade-B and Nissl stain). Minocycline significantly decreased both the microglial response and neuronal degeneration compared with the vehicle. Asphyxial CA significantly enhanced proinflammatory cytokine and chemokine levels in hippocampus versus control (assessed by multiplex bead array assay), specifically tumor necrosis factor-α (TNF-α), macrophage inflammatory protein-1α (MIP-1α), regulated upon activation, normal T-cell expressed and secreted (RANTES), and growth-related oncogene (GRO-KC) ( P<0.05). Minocycline attenuated ACA-induced increases in MIP-1α and RANTES ( P<0.05). These data show that microglial activation and cytokine production are increased in immature brain after ACA. The beneficial effect of minocycline suggests an important role for microglia in selective neuronal death after pediatric ACA, and a possible therapeutic target.

Effects of HBO with reduction of iNOS and HIF -1α in motor neurons after transient spinal cord ischemia in rabbits

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S452-S452
Author(s):  
Noritaka Murakami ◽  
Masahiro Sakurai ◽  
Takashi Horinouchi ◽  
Jun Ito ◽  
Shin Kurosawa ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Motor Neurons ◽  
Spinal Cord Ischemia
Sign in / Sign up

Export Citation Format

Share Document