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.

Abstract 148: Zoniporide Combined with α-Methylnorepinephrine Appears Highly Effective for Resuscitation from Cardiac Arrest in a Rat Model of Ventricular Fibrillation

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Lorissa Lamoureux ◽  
Herbert K Whitehouse ◽  
Jeejabai Radhakrishnan ◽  
Raúl J Gazmuri
Keyword(s):  
Cardiac Arrest ◽  
Chest Compression ◽  
Rat Model ◽  
Myocardial Dysfunction ◽  
Spontaneous Circulation ◽  
Sprague Dawley ◽  
Survival Times ◽  
Highly Effective ◽  
Electrical Shocks ◽  
Novel Strategy

Background: We have reported in rat and swine models of cardiac arrest that sodium hydrogen exchanger isoform-1 (NHE-1) inhibition facilitates resuscitation, ameliorates myocardial dysfunction, and improves survival. Others have reported that α-methylnorepinephrine (α-MNE) - a selective α2-adrenoreceptor agonist - is superior to epinephrine given its lack of β-agonist effects. We examined in a rat model of VF and closed-chest resuscitation the effects of combining the NHE-1 inhibitor zoniporide (ZNP) with α-MNE. Methods: VF was electrically induced in 32 male retired breeder Sprague-Dawley rats and left untreated for 8 minutes after which resuscitation was attempted by an 8 minute interval of chest compression and delivery of electrical shocks. Rats were randomized 1:1:1:1 to receive a 3 mg/kg bolus of ZNP or 0.9% NaCl before starting chest compression and a 100 μg/kg bolus of α-MNE or its vehicle at minute 2 of chest-compressions establishing 4 groups of 8 rats each. Successfully resuscitated rats were monitored for 240 minutes. Results: The number of rats that had return of spontaneous circulation and then survived 240 min were: α-MNE(-)/ZNP(-) 4 and 2; α-MNE(-)/ZNP(+) 5 and 5; α-MNE(+)/ZNP(-) 2 and 1; and α-MNE(+)/ZNP(+) 7 and 7 yielding a statistically significant effect on overall survival times corresponding to 105 ± 114, 150 ± 124, 58 ± 108, and 210 ± 85 min, respectively (p < 0.045). Post-resuscitation lactate levels were attenuated in all treatment groups with the greatest effect by the α-MNE(+)/ZNP(+) combination without major differences in hemodynamic function (Table). Conclusion: We confirm a beneficial effect resulting from the combination of ZNP (given to attenuate myocardial reperfusion injury) and α-MNE (given to augment peripheral vascular resistance during chest compression without the detrimental actions of epinephrine). The proposed combination may prove to be a highly effective novel strategy for resuscitation from cardiac arrest.

Abstract 179: Effects of Necrosulfonamide on Post-Resuscitation Survival and Neurological Function in a Rat Model of Cardiac Arrest

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Fenglian He ◽  
Guanghui Zheng ◽  
Juntao Hu ◽  
Weiwei Ge ◽  
Xianfei Ji ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Interleukin 1 ◽  
Kinase Domain ◽  
Spontaneous Circulation ◽  
Neurological Function ◽  
Protective Effects ◽  
Sprague Dawley ◽  
Injection Duration ◽  
Cerebral Ischemia And Reperfusion

Introduction: Gasdermin D (GSDMD), a previously unknown protein, serves as a key effector in pyroptosis and its inhibition has protective effects during cerebral ischemia and reperfusion. Necrosulfonamide (NSA) specifically blocks the mixed lineage kinase domain-like pseudo kinase (MLKL), which directly binds to GSDMD preventing pyroptotic cell death and interleukin-1 (IL-1) release. In this study, we investigated the effects of NSA on survival and neurological function after cardiac arrest and resuscitation. Hypothesis: Administration of NSA following cardiopulmonary resuscitation (CPR) will improve survival and neurological function in a rat model of cardiac arrest. Methods: Twelve male Sprague-Dawley rats weighting between 450-550g were utilized. Ventricular fibrillation was induced and untreated for 6 min followed by defibrillation after 8 min of CPR. Animals were then randomized into two groups: NSA and control. NSA (10mg/kg) or vehicle was administered 5 minutes after restoration of spontaneous circulation (ROSC) by intraperitoneal injection. Duration of survival and neurological deficit scores were recorded at 24, 48, and 72 hours after ROSC. Results: All animals were resuscitated successfully. Duration of survival was significantly longer in the NSA group compared to control (p<0.05, Figure 1). The severity of post-resuscitation cerebral dysfunction was significantly reduced in the NSA group compared to control (p<0.05, Figure 2). Conclusion: Administration of NSA after ROSC improves post-resuscitation survival and neurological function in a rat model of cardiac arrest.

Abstract 140: Effects of ω-3 Polyunsaturated Fatty Acids on Systemic Inflammation and Post-resuscitation Myocardial Function in a Rat Model of Cardiac Arrest and Cardiopulmonary Resuscitation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Cheng Cheng ◽  
Hui Li ◽  
Tao Jin ◽  
Lian Liang ◽  
Guozhen Zhang ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Cardiac Arrest ◽  
Polyunsaturated Fatty Acids ◽  
Systemic Inflammation ◽  
Rat Model ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Spontaneous Circulation ◽  
Sprague Dawley ◽  
Tnf Α

Introduction: Massive systemic inflammation is a primary cause of myocardial dysfunction following cardiac arrest (CA) and resuscitation (CPR). We investigated the effects of ω-3 polyunsaturated fatty acids (ω-3 PUFA) on systemic inflammation and myocardial function after CA and CPR. Hypothesis: Administration of ω-3 PUFA at the start of CPR will alleviate post CPR inflammation and improve cardiac function in a rat model of CA and CPR. Methods: 18 male Sprague-Dawley rats weighing between 450g-550g were randomized into three groups: Sham, Control, and ω-3 PUFA. Ventricular fibrillation (VF) was induced and untreated for 6 min. 4J defibrillation was attempted after 8 min of CPR. Saline placebo or ω-3 PUFA (5mL/kg) was infused at the start of CPR and continued for 4h. Ejection fraction (EF), cardiac output (CO) and myocardial performance index (MPI) were measured by echocardiography at baseline, 1, 3 and 6h after return of spontaneous circulation (ROSC). Inflammatory cytokines (IL-6 and TNF-α) and cardiac biomarker (cTnI) levels in plasma were detected at baseline and 6 hrs after ROSC. Results: A decrease in EF and CO and an increase in MPI occurred after resuscitation. Significant improvement was noted in ω-3 PUFA compared to control animals (p<0.05) (Fig. 1). ELISA analysis showed increased plasma IL-6, TNF-α, and cTnI in post-resuscitated rats. Administration of ω-3 PUFA attenuated the rise in these plasma biomarkers (p<0.05) (Fig. 2). Conclusion: Administration of ω-3 PUFA attenuates post-resuscitation systemic inflammation and improves myocardial function in a rat model of CA and CPR.

scholarly journals Modification of T cells function after restoration of spontaneous circulation in a rat model of cardiac arrest

2019 ◽  
Author(s):  
Chunlin Xing ◽  
Yang Chen ◽  
Xuemei Zhu ◽  
Guoping Lu ◽  
Weiming Chen
Keyword(s):  
T Cells ◽  
Cardiac Arrest ◽  
Rat Model ◽  
Spontaneous Circulation ◽  
Control Group ◽  
Sprague Dawley ◽  
Surface Molecules ◽  
Number Of Patients ◽  
Ifn Γ ◽  
Inhibitory Molecules

AbstractCardiac arrest (CA) is a prominent cause of mortality worldwide. A large number of patients after post-cardiac arrest is often associated with a phase of impaired immunity. Through an asphyxial cardiac arrest rat model, we investigate the peripheral blood T cells subsets and the expressions of surface molecules after restoration of spontaneous circulation (ROSC). Sprague-Dawley rats (weight, 300-400 g) were randomly divided into cardiac arrest (CA) group and sham-operated group. CA group rats were induced by 6 minutes of asphyxia. After successful ROSC, 24 surviving rats in two groups were randomly assigned to be sacrificed (n = 8 per subgroup) at 3, 24 and 72 h. The proportion of T cells and CD4+, CD8+ subsets as well as the expression of surface molecules (CTLA-4, PD-1, CD28) on T cells were identified by flow cytometry. The protein concentrations of cytokines (TNF-α, IL-6, IL-10, IL-4, IFN-γ, IL-17A) in serum were measured by ELISA. Compared with sham-operated control group, CD3+ lymphocytes in CA group were significantly decreased at 24 and 72 h post-ROSC. The expression levels of CD28, PD-1, and CTLA-4 on T cells were markedly increased in CA groups at 24 h post-ROSC. Additionally, the concentrations of IFN-γ were significantly declined, while IL-4 was markedly elevated in the CA group at 24 and 72 h post-ROSC. T cells function is moderately changed after CA, which is associated with decreased percentage of T cells, the upregulation of co-inhibitory molecules, and the shift from T helper (Th) 1 to Th2.

Abstract 211: UAMC-3203 Reduces the Severity of Post-resuscitation Myocardial Dysfunction in a Rat Model of Cardiac Arrest and Cardiopulmonary Resuscitation

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Tao Jin ◽  
Cheng Cheng ◽  
Hui Li ◽  
Lian Liang ◽  
Guozhen Zhang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cardiopulmonary Resuscitation ◽  
Cardiac Function ◽  
Rat Model ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Specific Inhibitor ◽  
Spontaneous Circulation ◽  
Sprague Dawley

Introduction: Previous studies have demonstrated that ferroptosis, a newly defined iron-dependent cell death, mediates ischemia/reperfusion induced cardiomyopathy. However, it is unclear whether ferroptosis plays a role in post-resuscitation myocardial dysfunction (PRMD). This study investigated the effects of UAMC-3203, a novel analog of ferroptosis specific inhibitors, on myocardial function after cardiopulmonary resuscitation (CPR). Hypothesis: Administration of UAMC-3203 during CPR alleviates PRMD in a rat model of cardiac arrest (CA) and CPR. Methods: 18 male Sprague-Dawley rats weighing between 450-550g were randomized into 3 groups: 1) Sham, 2) Control, and 3) UAMC-3203 (5mg/kg, IP at start of precordial compression). Ventricular fibrillation (VF) was induced and continued for 6min. CPR was then initiated for 8min, after which defibrillation was attempted. Ejection fraction (EF), cardiac output (CO) and myocardial performance index (MPI) were measured by echocardiography at baseline, 15min, 1h, 3h and 6h respectively after return of spontaneous circulation (ROSC). Results: A significant reduction in cardiac function was observed after resuscitation. At 15 minutes after ROSC, ultrasound showed no difference in cardiac function between UAMC and control. However, at 1, 3, and 6 h after ROSC, UAMC significantly improved myocardial function (p<0.05) (Fig. 1). Conclusion: A ferroptosis-specific inhibitor, UAMC-3203, alleviated PRMD significantly in a rat of model of CA and CPR. Further study is needed to determine the benefit of this agent in larger animals and potential safety in humans before it can be tested in clinical resuscitation.

Epinephrine Administration in Lipid-Based Resuscitation in a Rat Model of Bupivacaine-Induced Cardiac Arrest

2015 ◽  
Vol 40 (3) ◽  
pp. 223-231 ◽  
Author(s):  
Zhousheng Jin ◽  
Yun Xia ◽  
Fangfang Xia ◽  
Cong Wu ◽  
Zhe Chen ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Epinephrine Administration ◽  
Induced Cardiac Arrest

Abstract 11029: Netrin-1 Alleviates Post-Resuscitation Myocardial Dysfunction in a Rat Model of Cardiac Arrest

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Lu Yin ◽  
Shen Zhao ◽  
JoongBum Moon ◽  
Peng Sun ◽  
Jiangang Wang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Rat Model ◽  
Myocardial Dysfunction ◽  
Saline Group ◽  
Control Group ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Group 2

Introduction: Post-resuscitation myocardial dysfunction has been recognized as one of the major causes of fatal outcomes after initial successful cardiopulmonary resuscitation (CPR). Previous research demonstrated that Netrin-1 improved post ischemic injury cardiac function via preservation of mitochondrial integrity. In the present study, we investigated the role of netrin-1 after cardiac arrest. Hypothesis: We hypothesized that the netrin-1 alleviated post-resuscitation myocardial dysfunction in a rat model of cardiac arrest. Methods: A total of sixteen male Sprague-Dawley rats (450-550 g) were randomized to two groups as follows: (1) Control group (C group); (2) Netrin-1 group (N group). Ventricular fibrillation was induced and untreated for 8 mins followed by 8 mins of CPR. Netrin-1 or saline were given at the onset of precordial compression. Ejection fraction (EF) was measured by echocardiography at baseline, 1,2,3 and 4 hours after ROSC. Results: Eight rats were resuscitated in the netrin-1 group and 7 rats were resuscitated in the saline group. In both groups, EF decreased after resuscitation when compared to the baseline (#p < 0.05). In the netrin-1 group, EF decreased from ( 68.1±3.4)% at baseline to (51.1±5.0)% at 1 hour post-resuscitation. In the saline group, EF decreased from (67.7±2.1)% at baseline to (44.5±5.3)% at 1 hr post-resuscitation. EF was better in the netrin-1 group than in the saline group at 2, 3 and 4 hours post-resuscitation (*p < 0.05) ( Figure 1). Conclusion: Netrin-1 alleviates post-resuscitation myocardial dysfunction in a rat model of cardiac arrest.

Abstract 83: Effect of Therapeutic Hypothermia on Oxygenation Index in Rat Model of Cardiac Arrest

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Haifang Yu ◽  
Lu Yin ◽  
Ping Gong ◽  
Jiangang Wang ◽  
Zhengfei Yang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Pulmonary Function ◽  
Therapeutic Hypothermia ◽  
Rat Model ◽  
Mild Hypothermia ◽  
Oxygenation Index ◽  
Spontaneous Circulation ◽  
Control Group ◽  
Sprague Dawley ◽  
Successful Resuscitation

Introduction: Therapeutic hypothermia improves the outcomes of cerebral function after resuscitation from cardiac arrest (CA). The effect of therapeutic hypothermia on post resuscitation pulmonary function, however, is less known. In the present study, we investigated the effect of therapeutic hypothermia on oxygenation index, a sensitive index of pulmonary function,in a rat model of cardiac arrest and resuscitation. Hypothesis: We hypothesize that during therapeutic mild hypothermia in a rat model of cardiac arrest, the pulmonary function following resuscitation is less impaired when compare to normothermia. Methods: Twenty-one male Sprague-Dawley rats were randomized into three groups: 1) control group (control, n=5): the normothermic rats only received anesthesia and the surgical procedure as the other groups without ventricular fibrillation (VF); 2) normothermia group (NT, n=7): the normothermic rats were subjected to induced VF for 8 mins followed by 8 mins of cardiopulmonary resuscitation (CPR); 3) Mild hypothermia group (HT, n=9): the rats were subjected to induced VF for 8 mins followed by 8 mins of CPR. Mild hypothermia of 33±0.5°C was started 5 mins after return of spontaneous circulation (ROSC) and maintained for 8 hrs. The oxygenation indexes were measured at baseline, 2, 4 or 8 hours after ROSC with a conventional blood gas analyzer (PHOX plus L; Nova Biomedical Corporation, Waltham, MA, USA). Results: Compared to the control group, the oxygenation indexes of both the NT and HT groups were significantly decreased at 2 hrs after ROSC. However, more significant reduction in oxygenation index was observed in the NT group (Figure). Conclusions: There is an early pulmonary dysfunction after successful resuscitation from cardiac arrest. Hypothermia reduces the impairment of pulmonary function.

scholarly journals Improved Early Postresuscitation EEG Activity for Animals Treated with Hypothermia Predicted 96 hr Neurological Outcome and Survival in a Rat Model of Cardiac Arrest

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Bihua Chen ◽  
Feng-Qing Song ◽  
Lei-Lei Sun ◽  
Ling-Yan Lei ◽  
Wei-Ni Gan ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Neurological Outcome ◽  
Cardiac Pacing ◽  
Aortic Pressure ◽  
Sprague Dawley ◽  
Burst Frequency ◽  
Eeg Activity ◽  
Favorable Neurological Outcome ◽  
Hypothermic Group

Purpose.To investigate the effect of hypothermia on 96 hr neurological outcome and survival by quantitatively characterizing early postresuscitation EEG in a rat model of cardiac arrest.Materials and Methods.In twenty male Sprague-Dawley rats, cardiac arrest was induced through high frequency transesophageal cardiac pacing. Cardiopulmonary resuscitation was initiated after 5 mins untreated arrest. Immediately after resuscitation, animals were randomized to either 2 hrs of hypothermia (N=10) or normothermia (N=10). EEG, ECG, aortic pressure, and core temperature were continuously recorded for 6 hrs. Neurological outcome was evaluated daily during the 96 hrs postresuscitation period.Results.No differences in the baseline measurements and resuscitation outcome were observed between groups. However, 96 hr neurological deficit score (204 ± 255 versus 500 ± 0,P=0.005) and survival (6/10 versus 0/10,P=0.011) were significantly better in the hypothermic group. Quantitative analysis of early postresuscitation EEG revealed that burst frequency and spectrum entropy were greatly improved in the hypothermic group and correlated with 96 hr neurological outcome and survival.Conclusion.The improved burst frequency during burst suppression period and preserved spectrum entropy after restoration of continuous background EEG activity for animals treated with hypothermia predicted favorable neurological outcome and survival in this rat model of cardiac arrest.

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