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 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 319: Mild Hypothermia Preserves Cerebral Cortex Microcirculation After Resuscitation in a Rat Model of Cardiac Arrest

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Ping Gong ◽  
Shen Zhao ◽  
Jiangang Wang ◽  
Jie Qian ◽  
Zhengfei Yang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Cerebral Cortex ◽  
Mild Hypothermia ◽  
Spontaneous Circulation ◽  
Flow Index ◽  
Control Group ◽  
Sprague Dawley ◽  
Oxygen Extraction Ratio ◽  
Significant Difference ◽  
Sham Control Group

Introduction: Mild hypothermia is one of the effective treatments in comatose patients after cardiac arrest. However, its neuroprotective mechanism is not fully clear. In the present study, we investigated the effect of mild hypothermia on cerebral cortex microcirculation and cerebral oxygen extraction ratio (CERO2). Hypothesis: Mild hypothermia is associated with an improved cerebral cortex microcirculation and a decreased CERO2. Methods: Twenty-five male Sprague-Dawley rats were randomized into 3 groups: hypothermic (HT, n=10), normothermic (NT, n=10) or sham control group (SC, n=5). Ventricular fibrillation was electrically induced and untreated for 8 mins, followed by 8 mins of precordial compressions and mechanical ventilations. Core temperature was reduced to 33±0.5°C at 14 mins after return of spontaneous circulation (ROSC) with a combination of ice packs, an electrical fan and a cooling blanket. The temperature was maintained at 33°C for 8 hrs. Hemodynamics, jugular venous and aortic blood gas, and cerebral cortex microcirculation were measured at baseline, 2, 4 and 8 hrs after ROSC. Results: Of the 20 experimental rats, 15 were successfully resuscitated. There was no significant difference in the rate of ROSC in the NT and HT groups (7/10 vs. 8/10; p>0.05). Microvascular flow index was significantly reduced at 2, 4 and 8 hrs after ROSC but was significantly improved by mild hypothermia (Figure 1). Mild hypothermia significantly reduced the CERO2 after ROSC (Figure 2). Conclusions: Mild hypothermia improves the cerebral cortex microcirculatory blood supply/oxygen uptake mismatching after ROSC, which may provide one additional mechanism of cerebral protection.

Abstract 104: N-Acetyl Cysteine Improves Post Reperfusion Myocardial Dysfunction in a Rat Model of Cardiac Arrest and Return of Spontaneous Circulation

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Fenglian He
Keyword(s):  
Cardiac Arrest ◽  
Ventricular Fibrillation ◽  
Rat Model ◽  
Myocardial Function ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Spontaneous Circulation ◽  
Control Group ◽  
Successful Resuscitation ◽  
Return Of Spontaneous Circulation

N-acetylcysteine improves post reperfusion myocardial dysfunction in a Rat Model of Cardiac Arrest and return of spontaneous circulation Introduction: Studies have demonstrated that N-acetylcysteine (NAC) can attenuate regional myocardial ischemia/reperfusion injury and improved myocardial dysfunction. However, it is not clear whether NAC could protect post reperfusion myocardial dysfunction (PRMD) after cardiac arrest (CA) and return of spontaneous circulation (ROSC). In this study, we investigated the effect of NAC on post reperfusion myocardial dysfunction in a rat model of CA and ROSC. Hypothesis: NAC reduces the severity of PRMD in a rat model of CA and ROSC. Method: Ten healthy male Sprague-Dawley rats weighting 450g–550g were utilized, and randomly divided into two groups: 1) control group; 2) NAC group (150mg/kg). Ventricular fibrillation (VF) was induced. After 8 mins of VF, CPR was initiated for 8 mins, and defibrillation was then attempted. Myocardial function was measured by echocardiography at baseline, 2, 4 and 6 hours after successful resuscitation. Result: Except one in the control group, all animals were resuscitated. Myocardial function of post-resuscitation was significantly decreased in all animals. However, myocardial function gradually improved in animals treated with NAC when compared with those in control groups (Figure). Conclusion: In a rat model of cardiac arrest, NAC improves post-resuscitation myocardial dysfunction Figure The post-resuscitation myocardial dysfunction. BL, baseline; VF, ventricular fibrillation; CO, cardiac output; EF, ejection fraction; MPI, myocardial performance index; CPR, cardiopulmonary resuscitation; C group,control group; N group, NAC intervention group; * p < 0.05.vs. the C group.

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 173: The Neuroprotective Effect Of JZL184 is Comparable With Therapeutic Hypothermia in a Rat Model of Cardiac Arrest

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Jing Xu ◽  
Guanghui Zheng ◽  
Juntao Hu ◽  
Weiwei Ge ◽  
Jennifer Bradley ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Rat Model ◽  
Neuroprotective Effect ◽  
Experimental Studies ◽  
Flow Index ◽  
Protective Effects ◽  
Cerebral Microcirculation ◽  
Sprague Dawley ◽  
Neuroprotective Effects

Introduction: JZL184 is a synthetic monoacylglycerol lipase inhibitor that reduces brain edema, infarct size and alleviates inflammation following cerebral ischemia in experimental studies. In this study, we compared its cerebral protective effects with therapeutic hypothermia following cardiopulmonary resuscitation (CPR) in a rat model. Hypothesis: JZL184 will have similar neuroprotective effects to therapeutic hypothermia after cardiac arrest (CA) by reducing brain and blood brain barrier (BBB) injury and preserving cerebral microcirculation following CPR. Methods: Thirty six male Sprague-Dawley rats weighing between 450-550 g were randomized: 1) control 2) hypothermia 3) JZL184. Ventricular fibrillation was induced and untreated for 6 min for all rats. Resuscitation was attempted with a 4 Joule defibrillation after 8 min of CPR. Immediately following resuscitation, either hypothermia (33+0.5 o C) or JZL184 (16 mg/k, IP) was administered. Cerebral microcirculation, S-100β, NSE and Evan’s Blue (EB) concentrations were analyzed at 6hrs after resuscitation. Results: NSE and S-100β levels were higher in control compared to hypothermia and JZL18 at 6hr post ROSC (p < 0.001) (Fig. 1). Compared with control, there was a significant decrease in brain permeability to EB in Hypothermia and JZL184 after 6hr post ROSC (p<0.001) (Fig. 2). Microvascular flow index (MFI) was reduced in control compared with hypothermia and JZL184 6hr post ROSC (p <0.01). Conclusions: JZL184 administered following resuscitation reduced brain and BBB injury and preserved cerebral microcirculation at 6 hr post arrest to the same extent as hypothermia in a rat model of cardiac arrest.

Abstract 10773: Curcumin Improves the Outcomes of Cardiopulmonary Resuscitation in a Rat Model of Cardiac Arrest

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Zhengfei Yang ◽  
Jiangang Wang ◽  
Lu Yin ◽  
Shen Zhao ◽  
Ziren Tang ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Placebo Group ◽  
Rat Model ◽  
Myocardial Function ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Dysfunction ◽  
Ischemia Reperfusion ◽  
Sprague Dawley ◽  
Successful Resuscitation ◽  
Pre Treatment

Introduction: Curcumin has been proven to provide potent protection of vital organs against regional ischemia reperfusion injury. In this study, we investigated the effects of curcumin on the outcomes of CPR in a rat model of cardiac arrest. Hypothesis: Curcumin reduces the severity of post-CPR myocardial dysfunction and prolong the duration of survival. Method: Sixteen male Sprague-Dawley rats weighing between 450-550g were randomized into two groups: 1) Placebo; 2) Curcumin (100 mg/kg) pre-treatment. Ventricular fibrillation (VF) was induced. After 8 mins of VF, CPR was initiated for 8 mins and defibrillation was then attempted. Myocardial function was measured by echocardiography at baseline and hourly for 4 hours following successful resuscitation. The duration of survival was observed for total 72 hours. Result: Six animals in the placebo group and seven in the curcumin group were successfully resuscitated. Post-resuscitation myocardial function was significantly impaired in all animals. However, myocardial function gradually improved 4 hours after resuscitation and was significantly better in the animals pre-treated with curcumin (Figure). Significantly shorter duration of survival of 40±29 hours was observed in the placebo group. Conclusion: In a rat model of cardiac arrest, curcuminim proves post-resuscitation myocardial dysfunction and prolongs the duration of survival.

Abstract 246: Therapeutic Hypothermia Mimicking Peptide Administration During Cardiopulmonary Resuscitation Improved Cardiac Arrest Survival in Swine

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Matt Oberdier ◽  
Jing Li ◽  
Dan Ambinder ◽  
Xiangdong Zhu ◽  
Sarah Fink ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Therapeutic Hypothermia ◽  
Venous Blood ◽  
Plasma Concentrations ◽  
Sudden Cardiac Arrest ◽  
The United States ◽  
Rapid Onset ◽  
Spontaneous Circulation ◽  
Control Group ◽  
Swine Model

Background: Out-of-hospital sudden cardiac arrest is a leading cause of death in the United States, affecting over 350,000 people per year with an overall survival rate around 10%. CPR, defibrillation, and therapeutic hypothermia are common resuscitation strategies, but hypothermia is difficult to implement timely to achieve survival benefit. A cell-permeable peptide TAT-PHLPP9c has been shown to alter metabolic pathways similar to hypothermia, and decreases the release of two biomarkers, taurine and glutamate, during the high osmotic stress of heart stunning and brain injury in a mouse arrest model. Hypothesis: TAT-PHLPP9c, given during CPR, enhances 24-hour survival in a swine ventricular fibrillation (VF) model. Methods: In 14 (8 controls and 6 treated) sedated, intubated, and mechanically ventilated swine, after 5 min of VF, ACLS with vest CPR and periodic defibrillations was performed. Venous blood samples were collected at baseline, after 2 min of CPR, and at 2 and 30 min after return of spontaneous circulation (ROSC). The animals were survived up to 24 hrs and plasma samples were analyzed for glutamate and taurine in 2 controls and 1 animal given peptide. Results: Three of the control animals had ROSC, but none survived for 24 hrs, while 4 of 6 treated animals achieved neurologically intact survival at 24 hrs (p < 0.02). Compared to baseline, both taurine and glutamate plasma concentrations increased in the control group, but the increase was reduced substantially by the peptide treatment at 30 min after ROSC (Figure). Conclusion: The use of the cooling mimicking peptide TAT-PHLPP9c administered during CPR significantly improved 24-hour survival in this swine model of cardiac arrest. It reduced the increase of cerebral and myocardial metabolic biomarkers, which encourages utilizing a strategy of cell-permeable peptides for intravenous administration for more rapid onset of hypothermia-like salutary effects than are possible with current CPR cooling devices.

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 280: Evaluation of Cerebral Blood Oxygenation by NIRS During Asphyxia Cardiac Arrest and Resuscitation in Rats

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Tsukasa Yagi ◽  
Koichiro Shinozaki ◽  
Yu Okuma ◽  
Tai Yin ◽  
Mitsuaki Nishikimi ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Near Infrared ◽  
Oxygenation Index ◽  
Spontaneous Circulation ◽  
Blood Oxygenation ◽  
Upper Cervical Spine ◽  
Sprague Dawley ◽  
Abrupt Increase ◽  
Cerebral Blood Oxygenation ◽  
End Tidal

Background: Clinical investigators have focused on the real-time evaluation of cerebral blood oxygenation (CBO) by near-infrared spectroscopy (NIRS) during cardiopulmonary resuscitation (CPR). A previous study showed that an abrupt increase of Oxy-hemoglobin (Hb) concentration and tissue oxygenation index (TOI) was associated with the timing of return of spontaneous circulation (ROSC). However, it is not clear how TOI decreases in cardiac arrest (CA) and increases by resuscitation. Therefore, this study aimed to assess CBO with asphyxia CA and its association with CPR to ROSC in rats Method: Male Sprague-Dawley rats were used. We attached NIRS (NIRO-200NX, Hamamatsu Photonics, Japan) from nasion to upper cervical spine in rats. 10-minute asphyxia was given to induce CA. After CA, mechanical ventilation was restarted, and manual CPR was performed. We examined the mean arterial pressure (MAP), end-tidal carbon dioxide (ETCO2), and Oxy/Deoxy-Hb and TOI. Results: Out of 12 rats, 9 obtained sustained ROSC. After the induction of asphyxia, TOI rapidly dropped, and as subsequent CPR was undergoing, Oxy-Hb, Deoxy-Hb, and TOI increased in synchrony with chest compressions. And then, an abrupt increase in MAP, ETCO2, and TOI observed at the time of ROSC. Conclusion: Recent CPR guidelines suggest a use of ETCO2 during CPR since its abrupt increase is a reasonable indicator of ROSC. TOI can be an alternative of ETCO2, and in addition, it has the potential to serve as monitoring CBO during CPR and subsequently in post-ROSC care.

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.

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