Abstract 217: Increased Oxidation of Amplex Red in Post-Cardiac Arrest Human and Rat Plasma Can Be Utilized as a Potential Marker of Injury Severity

Circulation ◽  
2019 ◽  
Vol 140 (Suppl_2) ◽  
Author(s):  
Muhammad Shoaib ◽  
Ann Iverson ◽  
Tai Yin ◽  
Lance B Becker ◽  
Junhwan KIM
Keyword(s):  
Hydrogen Peroxide ◽  
Cardiac Arrest ◽  
Injury Severity ◽  
Ischemia Reperfusion ◽  
University Hospital ◽  
Ros Generation ◽  
Ischemic Damage ◽  
Sprague Dawley ◽  
Amplex Red ◽  
Potential Marker

Introduction: Cardiac arrest (CA), an unexpected loss of appropriate electrical signaling in the heart, leads to a loss of blood circulation and decreased oxygen perfusion. Ischemia results in the generation of hydrogen peroxide and other reactive oxygen species (ROS), thereby causing damage to tissues. Currently, there are no available biomarkers to elucidate the severity of ischemic damage. Therefore, oxidation of the Amplex Red (AR) assay by ROS into its fluorescent product, resorufin, may be used as a marker to determine injury severity. Methods: Plasma isolated from human CA patients from North Shore University Hospital was obtained to determine ROS generation. A commercially available Amplex Red assay kit was used to measure the amount of resorufin produced after oxidation due to hydrogen peroxide, peroxynitrite, and other ROS. To verify our human findings, we arbitrarily assigned adult male Sprague-Dawley rats into three groups (control, 10 min cardiac arrest, and 20 min cardiac arrest) using our reliable asphyxia-induced cardiac arrest model. Results: Despite human variations, our data on human CA patients showed an increased amount of AR oxidation as a result of ischemia. Our 10 min CA rat experimental model verified that Amplex Red is capable of detecting hydrogen peroxide and peroxynitrite formation after ischemia. Rats with 20 mins of ischemia time also produced resorufin, confirming that ischemia induces AR oxidation. Removing horseradish peroxidase and adding catalase controls for hydrogen peroxide and peroxynitrite, which should decrease AR oxidation; however, we observed an increase in AR oxidation. Therefore, we added phenylmethyl sulfonyl acid (PMSF), an inhibitor of carboxylesterase, an enzyme also capable of oxidizing Amplex Red, which resulted in decreased AR oxidation. Conclusion: By accounting for peroxide and peroxynitrite species, the increase in Amplex Red oxidation in the plasma of cardiac arrest human patients and rats can be attributed to carboxylesterase activity. Our data corroborates the various mechanisms of AR oxidation in the setting of ischemia-reperfusion allowing the Amplex Red assay to be utilized as a potential tool for assessing the degree of ischemic damage resulting from 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.

scholarly journals Plasma metabolomics supports the use of long-duration cardiac arrest rodent model to study human disease by demonstrating similar metabolic alterations

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Muhammad Shoaib ◽  
Rishabh C. Choudhary ◽  
Jaewoo Choi ◽  
Nancy Kim ◽  
Kei Hayashida ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Human Disease ◽  
Injury Severity ◽  
Tca Cycle ◽  
Suitable Model ◽  
Metabolic Dysfunction ◽  
Sprague Dawley ◽  
Metabolic Alterations ◽  
Long Duration

AbstractCardiac arrest (CA) is a leading cause of death and there is a necessity for animal models that accurately represent human injury severity. We evaluated a rat model of severe CA injury by comparing plasma metabolic alterations to human patients. Plasma was obtained from adult human control and CA patients post-resuscitation, and from male Sprague–Dawley rats at baseline and after 20 min CA followed by 30 min cardiopulmonary bypass resuscitation. An untargeted metabolomics evaluation using UPLC-QTOF-MS/MS was performed for plasma metabolome comparison. Here we show the metabolic commonality between humans and our severe injury rat model, highlighting significant metabolic dysfunction as seen by similar alterations in (1) TCA cycle metabolites, (2) tryptophan and kynurenic acid metabolites, and (3) acylcarnitine, fatty acid, and phospholipid metabolites. With substantial interspecies metabolic similarity in post-resuscitation plasma, our long duration CA rat model metabolically replicates human disease and is a suitable model for translational CA research.

scholarly journals The Responses of Tissues from the Brain, Heart, Kidney, and Liver to Resuscitation following Prolonged Cardiac Arrest by Examining Mitochondrial Respiration in Rats

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Junhwan Kim ◽  
José Paul Perales Villarroel ◽  
Wei Zhang ◽  
Tai Yin ◽  
Koichiro Shinozaki ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Mitochondrial Respiration ◽  
Ischemia Reperfusion ◽  
Liver Mitochondria ◽  
Brain Mitochondria ◽  
Heart Mitochondria ◽  
Whole Body ◽  
Sprague Dawley ◽  
Respiration Activity ◽  
The Brain

Cardiac arrest induces whole-body ischemia, which causes damage to multiple organs. Understanding how each organ responds to ischemia/reperfusion is important to develop better resuscitation strategies. Because direct measurement of organ function is not practicable in most animal models, we attempt to use mitochondrial respiration to test efficacy of resuscitation on the brain, heart, kidney, and liver following prolonged cardiac arrest. Male Sprague-Dawley rats are subjected to asphyxia-induced cardiac arrest for 30 min or 45 min, or 30 min cardiac arrest followed by 60 min cardiopulmonary bypass resuscitation. Mitochondria are isolated from brain, heart, kidney, and liver tissues and examined for respiration activity. Following cardiac arrest, a time-dependent decrease in state-3 respiration is observed in mitochondria from all four tissues. Following 60 min resuscitation, the respiration activity of brain mitochondria varies greatly in different animals. The activity after resuscitation remains the same in heart mitochondria and significantly increases in kidney and liver mitochondria. The result shows that inhibition of state-3 respiration is a good marker to evaluate the efficacy of resuscitation for each organ. The resulting state-3 respiration of brain and heart mitochondria following resuscitation reenforces the need for developing better strategies to resuscitate these critical organs following prolonged cardiac arrest.

scholarly journals Elevated Plasma Soluble PD-L1 Levels in Out-of-Hospital Cardiac Arrest Patients

2021 ◽  
Vol 10 (18) ◽  
pp. 4188
Author(s):  
Miho Sumiyoshi ◽  
Eiji Kawamoto ◽  
Yuki Nakamori ◽  
Ryo Esumi ◽  
Kaoru Ikejiri ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Ischemia Reperfusion ◽  
Plasma Concentrations ◽  
Spontaneous Circulation ◽  
University Hospital ◽  
Soluble Form ◽  
Enzyme Linked Immunosorbent Assay ◽  
Immune Functions ◽  
Protein Levels ◽  
Hospital Cardiac Arrest

Background: A deregulated immune system has been implicated in the pathogenesis of post-cardiac arrest syndrome (PCAS). A soluble form of programmed cell death-1 (PD-1) ligand (sPD-L1) has been found at increased levels in cancer and sustained inflammation, thereby deregulating immune functions. Here, we aim to study the possible involvement of sPD-L1 in PCAS. Methods: Thirty out-of-hospital cardiac arrest (OHCA) patients consecutively admitted to the ER of Mie University Hospital were prospectively enrolled. Plasma concentrations of sPD-L1 were measured by an enzyme-linked immunosorbent assay in blood samples of all 30 OHCA patients obtained during cardiopulmonary resuscitation (CPR). In 13 patients who achieved return-of-spontaneous-circulation (ROSC), sPD-L1 levels were also measured daily in the ICU. Results: The plasma concentrations of sPD-L1 in OHCA were significantly increased; in fact, to levels as high as those observed in sepsis. sPD-L1 levels during CPR correlated with reduced peripheral lymphocyte counts and increased C-reactive protein levels. Of 13 ROSC patients, 7 cases survived in the ICU for more than 4 days. A longitudinal analysis of sPD-L1 levels in the 7 ROSC cases revealed that sPD-L1 levels occurred in parallel with organ failure. Conclusions: This study suggests that ischemia- reperfusion during CPR may aberrantly activate immune and endothelial cells to release sPD-L1 into circulation, which may play a role in the pathogenesis of immune exhaustion and organ failures associated with PCAS.

H2O2-Responsive Antioxidant Nanoparticle Attenuates Whole Body Ischemia/Reperfusion-Induced Multi-Organ Damages

2020 ◽  
pp. 107424842096957
Author(s):  
Ruijian Li ◽  
Sang Jae Rhee ◽  
Soochan Bae ◽  
Shi Su ◽  
Chang-Sun Kang ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiac Arrest ◽  
Ischemia Reperfusion ◽  
Spontaneous Circulation ◽  
Organ Injury ◽  
Whole Body ◽  
Ros Generation ◽  
Vanillyl Alcohol ◽  
Multiple Organs ◽  
Significant Difference

Mortality and morbidity after cardiac arrest remain high due to ischemia/reperfusion (I/R) injury causing multi-organ damages, even after successful return of spontaneous circulation. We previously generated H2O2-activatable antioxidant nanoparticles formulated with copolyoxalate containing vanillyl alcohol (PVAX) to prevent I/R injury. In this study, we examined whether PVAX could effectively reduce organ damages in a rat model of whole-body ischemia/reperfusion injury (WBIR). To induce a cardiac arrest, 70µl/100 g body weight of 1 mmol/l potassium chloride was administered via the jugular venous catheter. The animals in both the vehicle and PVAX-treated groups had similar baseline blood pressure. After 5.5 minutes of cardiac arrest, animals were resuscitated via intravenous epinephrine followed by chest compressions. PVAX or vehicle was injected after the spontaneous recovery of blood pressure was noted, followed by the same dose of second injection 10 minutes later. After 24 hours, multiple organs were harvested for pathological, biochemical, molecular analyses. No significant difference on the restoration of spontaneous circulation was observed between vehicle and PVAX groups. Analysis of organs harvested 24 hours post procedure showed that whole body I/R significantly increased reactive oxygen species (ROS) generation, inflammatory markers, and apoptosis in multiple organs (heart, brain, and kidney). PVAX treatment effectively blocked ROS generation, reduced the elevation of pro-inflammatory cytokines, and decreased apoptosis in these organs. Taken together, our results suggest that PVAX has potent protective effect against WBIR induced multi-organ injury, possibly by blocking ROS-mediated cell damage.

Abstract P133: Role of Akt and p38 in Oxidant Stress Injury and Hypothermic Protection in Murine Cardiomyocytes

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Kimberly R Wojcik ◽  
Zuo-Hui Shao ◽  
Chang-Qing Li ◽  
Kimm J Hamann ◽  
Terry L Vanden Hoek
Keyword(s):  
Cell Death ◽  
Cardiac Arrest ◽  
Cell Injury ◽  
Ischemia Reperfusion ◽  
Oxidant Stress ◽  
Ros Generation ◽  
Akt Inhibitor ◽  
Stress Injury ◽  
P38 Inhibitor ◽  
Sb 203580

Cardiac arrest is an ischemia/reperfusion (I/R) disease characterized by oxidant generation, inflammation, and cell death; and hypothermia (HT) has been shown to improve post-cardiac arrest reperfusion injury. We developed a neonatal mouse cardiomyocyte model of I/R (90 min I + 3 hr R) that demonstrates cell injury associated with increased reactive oxygen species (ROS) generation at reperfusion (as measured by DCFH). Mild HT (32°C) protects mouse cardiomyocytes from I/R injury, and we hypothesize that this protection may be related to the activation of the survival kinase Akt. The Akt inhibitor API-2 (10 ìM) reversed HT protection [32.4 ± 7.1% vs 65.7 ± 6.3% with API-2, p< .01(as measured by PI)] to cell death levels commensurate with normothermic I/R injury (60.7 ± 6.0%). Phospho-Akt (pAkt) levels declined during ischemia, and while both Ser473 and Thr308 were phosphorylated in normothermia and HT within 15 min reperfusion, HT showed an augmented level of pAkt at Thr308. Furthermore, this increase was sustained for the first 30 min of reperfusion. To further study this relationship, murine cardiomyocytes were exposed to exogenous H2O2 to mimic the oxidant stress associated with I/R. Mouse cardiomyocytes demonstrated a dose- and time-dependent activation of Akt to H2O2 that showed maximal activation of both the Ser473 and Thr308 sites within 30 min with 200 ìM H2O2. As in I/R-stimulated cells, the Thr308 site declined to near baseline levels within 1 hr while Ser473 remained elevated. Based on recent findings linking Akt and ROS with p38, we examined the effect of I/R and H2O2 on p38. Mouse cardiomyocytes demonstrated a rapid activation of p-p38 (Thr10/Tyr182) in the context of both stresses. Further, we studied the effect of the Akt inhibitor, API-2, as well as the p38 inhibitor, SB 203580, in H2O2-stimulated cells. As in I/R, API-2 blocked H2O2-induced pAkt, but this inhibitor did not have any effect on p-p38. However, when p38 activation was blocked using SB 203580, pAkt levels decreased by 2 hr. These data suggest that HT is, in part, mediated through Akt and that p38 lies upstream of Akt in the context of oxidant stress. These kinases may act as triggers for the initiation of survival pathways in cardiomyocytes to combat potential damage induced by ROS generation.

Abstract P34: Nitrite Therapy upon Resuscitation from Cardiac Arrest Reversibly Inhibits Mitochondrial Complex I Reducing ROS Burst and Improving Cardiac Function and Survival

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Cameron Dezfulian ◽  
Sruti Shiva ◽  
Akshay Pendyal ◽  
Aleksey Alekseyenko ◽  
Stasia A Anderson ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Complex I ◽  
Myocardial Dysfunction ◽  
Cardiac Contractility ◽  
Respiratory Control ◽  
Chain Complex ◽  
Ros Generation ◽  
Atp Production ◽  
Amplex Red ◽  
Ros Burst

Nitrite reversibly S-nitrosates mitochondrial electron transport chain complex I (cxI) resulting in transient inhibition and reduction of pathological ROS burst after ischemia. We hypothesized that nitrite therapy at CPR initiation could thus improve cardiac contractility and mortality. Anesthetized C57BL/6 mice underwent hyperkalemic cardiac arrest maintained for 12min at 36.5C prior to randomly receiving blinded IV nitrite or saline placebo, epinephrine, chest compressions and ventilation for up to 150 sec. ROSC was obtained in excess of 90% in both groups. Hearts were excised just prior to asystole, 5 or 60 minutes after the initiation of CPR and mitochondria isolated. Respiration was assessed by oxygen consumption after providing the cxI substrate pyruvate or the complex II (cxII) substrate succinate. CxI activity was directly assayed by NADH oxidation, peroxide generation measured by Amplex Red peroxidation and ATP production quantified by luciferin luminescence. Nitrite therapy was associated with improved hemodynamics and significantly improved LVEF and RVEF (Table 1 ) and better 22h survival (HR 2.72 [95% CI:1.1– 6.7]). Nitrite significantly reduced cxI mediated respiration 5 min post-CPR with loss of inhibition by 60min based on respiration and ATP production (Table II ). Respiration efficiency (respiratory control ratio) did not change, nor was there significant cxII inhibition. Early cxI inhibition was associated with significantly less ROS. Nitrite therapy transiently and reversibly inhibits cxI reducing reperfusion ROS-mediated injury and resulting in less myocardial dysfunction and death after cardiac arrest. Myocardial dysfunction occurs after cardiac arrest and is reduced with nitrite therapy Nitrite therapy specifically and reversibly inhibits complex I and reduces ROS generation

Abstract 155: Identification of Decreased Plasma Lysophosphatidylcholine Using Phospholipidomics in Cardiac Arrest: A Novel Therapeutic Application

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_4) ◽  
Author(s):  
Mitsuaki Nishikimi ◽  
Tsukasa Yagi ◽  
Ryosuke Takegawa ◽  
Shoaib Muhammad ◽  
Kei Hayashida ◽  
...  
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Brain Function ◽  
Injury Severity ◽  
University Hospital ◽  
Control Group ◽  
Therapeutic Application ◽  
Public Health Burden ◽  
Plasma Phospholipids ◽  
Novel Therapeutic

Introduction: Cardiac arrest (CA) is a significant public health burden with few effective therapies available. Plasma phospholipids are important for proper organ function. We hypothesized that alterations in plasma phospholipids may play an important role in the pathophysiology of CA and normalizing these alterations may be a novel therapeutic application for the treatment of CA. Objective: The aim of this study was to test the phospholipid therapy as a novel therapeutic approach in CA. Methods and Results: We performed phospholipidomics on plasma samples from CA patients and controls from North Shore University Hospital to identify plasma phospholipids that correlate with injury severity. We then confirmed the finding using our rat model of 10 and 14 min of asphyxia-induced CA. Finally, we tested the effect of administering LPC using the same model. From the phospholipids analyzed, lysophosphatidylcholine (LPC) levels were found to be the most significantly decreased in CA patients, which was also associated with survival of patients. The same trend was observed in the rat model where rats after 14 min CA had significantly lower plasma LPC levels than rats after 10 min CA. We also found that LPC levels began to decrease continuously following resuscitation, but not during the ischemic phase of CA. Finally, we found that LPC administration substantially increased rat survival compared to the control group. Rats who survived in the LPC-treated group displayed significantly improved brain function and the neuroprotective effect of LPC is supported by improved brain histology. We also found LPC treatment increased plasma IL-10 levels and decreased IL-6 levels post-CA. Conclusion: Plasma LPC levels inversely correlated with survival and LPC treatment significantly improved brain function and rat survival. This data indicates that the decrease of plasma LPC is a major mechanism responsible for brain damage demonstrating the potential of LPC as a novel therapeutic in CA.

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.

Abstract 298: Identification of LncRNA-miRNA-mRNA Network in Myocardium After Successful Resuscitation in a Rat Model of Prolonged Cardiac Arrest

Circulation ◽  
2018 ◽  
Vol 138 (Suppl_2) ◽  
Author(s):  
Jingying Hou ◽  
Zhengfei Yang ◽  
Wanchun Tang
Keyword(s):  
Cardiac Arrest ◽  
Rat Model ◽  
Regulatory Network ◽  
High Throughput Sequencing ◽  
Ischemia Reperfusion Injury ◽  
Myocardial Dysfunction ◽  
Expression Profiles ◽  
Ischemia Reperfusion ◽  
Sprague Dawley ◽  
Successful Resuscitation

Introduction: Previous studies have indicated that lncRNA participates in regional myocardial ischemia-reperfusion injury (IRI). However, the lncRNA-miRNA-mRNA crosstalk in the global myocardial IRI, which is implicated in the pathophysiology of post-resuscitation myocardial dysfunction (PRMD), has still not been explored. Hypothesis: To identify lncRNA-miRNA-mRNA regulatory network in myocardium after successful resuscitation in a rat model of prolonged cardiac arrest. Methods: Six male Sprague Dawley rats were randomized into sham control and ventricular fibrillation (VF)-CPR groups, with three rats in each group. VF was induced and untreated for 8 minutes. Defibrillation was attempted after 8 minutes of CPR. Heart tissue was obtained at 6 hours after resuscitation and lncRNA, miRNA and mRNA expression profiles were examined by using high-throughput sequencing. LncRNA-miRNA-mRNA interaction network was predicted and constructed. Results: Numbers of differentially expressed (DE) lncRNA, miRNA and mRNA were detected (Fig 1A). LncRNAs co-located or co-expressed target mRNAs and DE mRNAs were revealed (Fig 1B). The intersection of DE mRNAs with targeted mRNA of DE miRNAs was made (Fig 1C). A total of 129 feed forward loops were predicted as lncRNA-associated ceRNA networks,with 126 lncRNA (up)-miRNA (down)-mRNA (up) and 3 lncRNA (down)-miRNA (up)-mRNA (down) (Fig 2). Conclusions: LncRNA-miRNA-mRNAs network was predicted and constructed in myocardium after successful resuscitation in a rat model of prolonged cardiac arrest. Further exploration into the specific functional roles of the ceRNA regulatory network will be conducive for the treatment of PRMD.

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