scholarly journals Retraction of: Abstract 03: High-Dose Intranasal Insulin During CPR Improves Neurological Outcomes in a Rat Model of Cardiac Arrest

Circulation ◽  
2021 ◽  
Vol 144 (21) ◽  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
High Dose ◽  
Intranasal Insulin ◽  
Neurological Outcomes

Abstract 03: High-Dose Intranasal Insulin During CPR Improves Neurological Outcomes in a Rat Model of Cardiac Arrest

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Tulasi Jinka ◽  
Adam D Chalek ◽  
Joseph M Wider ◽  
Kathleen J Maheras ◽  
Amanda Qvigstad ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Therapeutic Window ◽  
Mechanistic Study ◽  
High Dose ◽  
Intranasal Insulin ◽  
Long Term Outcome ◽  
Neurologic Function ◽  
Survival Signaling ◽  
Asphyxial Cardiac Arrest

Introduction: Post-cardiac arrest brain injury is a major cause of mortality and morbidity. Insulin has well-established CNS neuroprotecive properties mediated by the AKT survival signaling pathway, and known transnasal transport mechanisms make it possible to rapidly achieve therapeutic brain insulin levels after intranasal delivery. Hypothesis: We hypothesize that high-dose intranasal insulin (HD-IN-I) administered during CPR, could improve neurologic outcomes in a rat model of asphyxial cardiac arrest. Methods: Male Long Evans rats were subjected to 8-minute asphyxial cardiac arrest then block randomized to HD-IN-I (1.92 U/g brain wet weight) or placebo (PL) given at the onset of CPR by an experimental operator blinded to treatment. Sham operated rats were used as uninjured controls. For the long-term outcome study (n = 14/group), rats with return of spontaneous circulation (ROSC) were maintained at 37.0 ±0.5 °C for 72 hours and neurologic function was assessed on days 7 - 10. For the mechanistic study (n = 6/group), rats with ROSC were euthanized 30 minutes after ROSC and regional brain homogenates were analyzed by western blot for AKT phosporylation. Results: HD-IN-I during CPR had no statistically significant effect on ROSC rate (93% (13/14) HD-IN-I vs. 86% (12/14) PL, p > 0.05) or 10-day survival (71% (10/14) HD-INI vs. 43% (6/14) PL, p > 0.05). HD-IN-I had no significant impact on serum glucose concentrations. At 10 days post-ROSC, rats in the HD-IN-I group had significantly improved performance on rotarod (latency to fall 87±27 sec HD-IN-I vs. 41±18 sec PL, p < 0.05), Barnes maze (latency to escape box 27±15 sec HD-IN-I vs. 298±5 sec PL, p < 0.05), and passive avoidance (latency to re-enter shock chamber 300±0 sec HD-IN-I vs. 142±46 sec PL, p < 0.05) testing. Hippocampal phosph-AKT/total AKT ratio increased 2-fold in the placebo group and 5.7-fold in the HD-IN-I group relative to shams (p < 0.05). Conclusions: HD-IN-I administered during CPR causes rapid activation of brain AKT survival signaling and improves recovery of neurologic function in a rat cardiac arrest model. Additional studies are warranted to determine dose optimization, therapeutic window and effectiveness in large animal models to advance this novel therapy toward clinical trials.

scholarly journals Melatonin improves neurological outcomes and preserves hippocampal mitochondrial function in a rat model of cardiac arrest

PLoS ONE ◽  
2018 ◽  
Vol 13 (11) ◽  
pp. e0207098 ◽  
Author(s):  
Linghui Yang ◽  
Jing Wang ◽  
Yan Deng ◽  
Cansheng Gong ◽  
Qin Li ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Mitochondrial Function ◽  
Neurological Outcomes

scholarly journals Inhaling Hydrogen Ameliorates Early Postresuscitation EEG Characteristics in an Asphyxial Cardiac Arrest Rat Model

2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Gang Chen ◽  
Jingru Li ◽  
Jianjie Wang ◽  
Bihua Chen ◽  
Yongqin Li
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Animal Studies ◽  
Onset Time ◽  
Quantitative Eeg ◽  
Permutation Entropy ◽  
Sprague Dawley ◽  
Ctrl Group ◽  
Neurological Outcomes ◽  
Prognostic Accuracy

Background. Electroencephalography (EEG) is commonly used to assess the neurological prognosis of comatose patients after cardiac arrest (CA). However, the early prognostic accuracy of EEG may be affected by postresuscitation interventions. Recent animal studies found that hydrogen inhalation after CA greatly improved neurological outcomes by selectively neutralizing highly reactive oxidants, but the effect of hydrogen inhalation on EEG recovery and its prognostication value are still unclear. The present study investigated the effects of hydrogen inhalation on early postresuscitation EEG characteristics in an asphyxial CA rat model. Methods. Cardiopulmonary resuscitation was initiated after 5 min of untreated CA in 40 adult female Sprague-Dawley rats. Animals were randomized for ventilation with 98% oxygen plus 2% hydrogen (H2) or 98% oxygen plus 2% nitrogen (Ctrl) under normothermia for 1 h. EEG characteristics were continuously recorded for 4 h, and the relationships between quantitative EEG characteristics and 96 h neurological outcomes were investigated. Results. No differences in baseline and resuscitation data were observed between groups, but the survival rate was significantly higher in the H2 group than in the Ctrl group (90% vs. 40%, P<0.01). Compared to the Ctrl group, the H2 group showed a shorter burst onset time (21.85 [20.00–23.38] vs. 25.70 [22.48–30.05], P<0.01) and time to normal trace (169.83 [161.63–208.55] vs. 208.39 [186.29–248.80], P<0.01). Additionally, the burst suppression ratio (0.66 ± 0.09 vs. 0.52 ± 0.17, P<0.01) and weighted‐permutation entropy (0.47 ± 0.16 vs. 0.34 ± 0.13, P<0.01) were markedly higher in the H2 group. The areas under the receiver operating characteristic curves for the 4 EEG characteristics in predicting survival were 0.82, 0.84, 0.88, and 0.83, respectively. Conclusions. In this asphyxial CA rat model, the improved postresuscitation EEG characteristics for animals treated with hydrogen are correlated with the better 96 h neurological outcome and predicted survival.

scholarly journals The effect of high-dose intramuscular epinephrine on the recovery of spontaneous circulation in an asphyxia‐induced cardiac arrest rat model

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Daesung Lim ◽  
Soo Hoon Lee ◽  
Dong Hoon Kim ◽  
Changwoo Kang ◽  
Jin Hee Jeong ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Saline Group ◽  
Spontaneous Circulation ◽  
Rank Test ◽  
High Dose ◽  
Sprague Dawley ◽  
Epinephrine Administration ◽  
Arterial Blood ◽  
Induced Cardiac Arrest

Abstract Background Obtaining vascular access can be challenging during resuscitation following cardiac arrest, and it is particularly difficult and time-consuming in paediatric patients. We aimed to compare the efficacy of high-dose intramuscular (IM) versus intravascular (IV) epinephrine administration with regard to the return of spontaneous circulation (ROSC) in an asphyxia-induced cardiac arrest rat model. Methods Forty-five male Sprague-Dawley rats were used for these experiments. Cardiac arrest was induced by asphyxia, and defined as a decline in mean arterial pressure (MAP) to 20 mmHg. After asphyxia-induced cardiac arrest, the rats were randomly allocated into one of 3 groups (control saline group, IV epinephrine group, and IM epinephrine group). After 540 s of cardiac arrest, cardiopulmonary resuscitation was performed, and IV saline (0.01 cc/kg), IV (0.01 mg/kg, 1:100,000) epinephrine or IM (0.05 mg/kg, 1:100,000) epinephrine was administered. ROSC was defined as the achievement of an MAP above 40 mmHg for more than 1 minute. Rates of ROSC, haemodynamics, and arterial blood gas analysis were serially observed. Results The ROSC rate (61.5%) of the IM epinephrine group was less than that in the IV epinephrine group (100%) but was higher than that of the control saline group (15.4%) (log-rank test). There were no differences in MAP between the two groups, but HR in the IM epinephrine group (beta coefficient = 1.02) decreased to a lesser extent than that in the IV epinephrine group with time. Conclusions IM epinephrine induced better ROSC rates compared to the control saline group in asphyxia-induced cardiac arrest, but not compared to IV epinephrine. The IM route of epinephrine administration may be a promising option in an asphyxia-induced cardiac arrest.

scholarly journals Improving neurological outcomes post-cardiac arrest in a rat model: Immediate hypothermia and quantitative EEG monitoring

Resuscitation ◽  
2008 ◽  
Vol 76 (3) ◽  
pp. 431-442 ◽  
Author(s):  
Xiaofeng Jia ◽  
Matthew A. Koenig ◽  
Hyun-Chool Shin ◽  
Gehua Zhen ◽  
Carlos A. Pardo ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Quantitative Eeg ◽  
Eeg Monitoring ◽  
Neurological Outcomes

scholarly journals Post‐Cardiac Arrest Hydrocortisone Use Ameliorates Cardiac Mitochondrial Injury in a Male Rat Model of Ventricular Fibrillation Cardiac Arrest

2021 ◽  
Author(s):  
Min‐Shan Tsai ◽  
Chien‐Hua Huang ◽  
Chen‐Hsu Wang ◽  
Hsaio‐Ju Cheng ◽  
Shih‐Ni Wu ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Rat Model ◽  
Low Dose ◽  
Myocardial Damage ◽  
Male Rat ◽  
Control Group ◽  
High Dose ◽  
Mitochondrial Injury ◽  
Treatment Groups

Background Steroid use after cardiac arrest has been reported to improve survival and neurological outcome in cardiac arrest survivors. The study aimed to evaluate the effect of post‐arrest hydrocortisone use on myocardial damage and cardiac mitochondrial injury in a rat model of ventricular fibrillation cardiac arrest. Methods and Results Ventricular fibrillation cardiac arrest was induced and left untreated for 5 minutes in adult male Wistar rats. Cardiopulmonary resuscitation and electric shocks were then applied to achieve return of spontaneous circulation (ROSC). Successfully resuscitated animals were randomized into 3 groups: control, low‐dose hydrocortisone (2 mg/kg), and high‐dose hydrocortisone (8 mg/kg). The low‐dose hydrocortisone and high‐dose hydrocortisone (treatment) groups received intravenous hydrocortisone immediately after ROSC and the control group received saline as placebo. Each group consisted of 15 animals. Within 4 hours of ROSC, both treatment groups showed a higher cardiac output than the control group. At the fourth hour following ROSC, histological examination and transmission electron microscopy demonstrated less myocardial damage and mitochondrial injury in the animals treated with hydrocortisone. In the treatment groups, hydrocortisone mitigated the acceleration of Ca 2+ ‐induced mitochondrial swelling and suppression of complex activity observed in the control group. At the 72nd hour after ROSC, a significantly higher proportion of animals treated with hydrocortisone survived and had good neurological recovery compared with those given a placebo. Conclusions Hydrocortisone use after cardiac arrest may mitigate myocardial injury and cardiac mitochondrial damage and thus improve survival, neurological and histological outcomes in a rat model of ventricular fibrillation cardiac arrest.

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