BACKGROUND:Cardiac fibroblasts (CFs) are essential for cardiac morphogenesis and homeostasis. We investigated whether transcription factor EB (TFEB) directly targeted and suppressed the activation of CFs, aiming to elucidate its underlying pathological mechanism from the perspectives of gene and cell therapy. METHODS:Following myocardial infarction (MI) induction, we performed transcriptome sequencing of CFs isolated from R26-LSL-TFEB+/+; Acta2-cre (n = 3) and R26-LSL-TFEB+/+ (n = 3) mice. Differential gene expression and functional enrichment analyses were conducted using R software. The binding between TFEB and Thrombospondin-1 (Thbs1) was validated by ChIP-qPCR assay. CFs were extracted from adult mice in the R26-LSL-TFEB+/+; Acta2-cre and R26-LSL-TFEB+/+ groups. Protein expressions of integrin, CD47, CD36, Thbs1, p-paxillin, vinculin, P-FAK, and α- SMA were detected by Western blot. Cell migration was assessed by the wound healing and Transwell assays. RESULTS:TFEB modulated the expression of a broad spectrum of RNAs associated with the transformation of CFs. Pathway analysis revealed significant enrichment in pathways related to extracellular matrix (ECM) receptor interaction and focal adhesion (FA). Notably, both mRNA and protein levels of Thbs1 were markedly elevated in TFEB-overexpressing CFs. Integrated computational prediction and chromatin immunoprecipitation assays identified that TFEB directly bound to the promoter region of Thbs1. This binding was associated with downstream modulation of its receptor network and a concomitant reduction in FA complex activation at the protein level. These findings positioned Thbs1 as a key transcriptional target through which TFEB regulated ECM-related signaling and cellular adhesion dynamics in CFs. DISCUSSION:The current findings showed that the modulation of Thbs1 and associated FA signaling was a mechanism through which TFEB overexpression exerted its anti-fibrotic effects on CFs. This highlighted the TFEB-Thbs1 axis as a potential novel target for developing therapeutic strategies to mitigate cardiac fibrosis. CONCLUSIONS:This study suggested that the protective effect of TFEB against MI injury was associated with the Thbs1/FA signaling pathway, providing a novel potential therapeutic target for cardiac fibrosis.

Objective: To investigate whether the histone deacetylase (HDAC) activator ITSA‐1 can ameliorate systemic inflammation after cardiac arrest (CA), thereby enhancing cardiac function and neurological outcomes in rats. Materials and Methods: Sixty‐nine healthy adult male Wistar rats were subjected to 12 min of CA induced by Vecuronium bromide. The rats were randomly assigned to five groups: normal control, sham operation, control, suberoylanilide hydroxamic acid (SAHA), and ITSA‐1. The study evaluated the effects of ITSA‐1 on cardiac function, survival, and neurological functions, including the neurological deficit score (NDS) at 24‐, 48‐, and 72‐h post‐return of spontaneous circulation (ROSC) and Morris water maze performance at 72 h. Additionally, levels of TNF‐ α , IL‐1 β , glial fibrillary acidic protein (GFAP), S100 β in plasma, and TNF‐ α , IL‐1 β in the hippocampus were measured 4 h post‐ROSC. Western blot analysis was used to assess HDACs, nuclear factor kappa B (NF‐ κ B), p‐NF‐ κ B, caspase‐3, cleaved caspase‐3, Bcl‐2, and Bax protein expressions. Results: ITSA‐1 reduced basic life support (BLS) duration and adrenaline dosage during cardiopulmonary resuscitation (CPR) and improved cardiac and neural functions, enhancing survival compared to the control and SAHA groups. ITSA‐1 decreased serum levels of IL‐1 β , TNF‐ α , GFAP, S100 β , and hippocampal TNF‐ α , IL‐1 β , promoting neuronal survival in the CA1 region. It also inhibited glial cell activation and reduced histone acetylation, blocking the NF‐ κ B pathway and neuronal apoptosis. Conclusion: ITSA‐1 enhances the recovery and survival of post‐ROSC rats by diminishing histone acetylation and mitigating systemic inflammation. This effect is possibly due to the inhibition of glial cell activation, increased neuronal survival in the brain, and improved cardiac output (CO) and ejection fraction (EF).

Background Therapeutic mild hypothermia (MH) is expected to improve the neurological outcome and the survival rate of CPR after cardiac arrest (CA). However, the mechanisms by which MH protects cardiomyocytes remain largely unexplored. Methods In this study, three- to four-month-old male Wistar rats, weighing between 319.1 and 480.0 grams, were randomly divided into normothermia (NT) groups (acceptable range, 36.0-38.0°C) and MH groups (acceptable range, 32-34°C). Ten minutes after CA, CPR was perfumed with a slow injection of 0.30-0.50 mL epinephrine solution (30.00 μg/mL). Moreover, to investigate the role of TRPV1, capsaicin was administered through the right femoral artery in both NT and MH groups. Results We found that MH improved the spontaneous breathing recovery, increased survival rate, and inhibited cardiac necroptosis in Wistar rats after CPR. Additionally, MH alleviated primary cardiomyocytes necroptosis after oxygen-glucose deprivation and reperfusion through upregulating TRPV1, downregulating EGFR, and subsequently suppressing MLKL. Furthermore, the combination of capsaicin, a TRPV1 activator, with MH enhanced blood pressure in Wistar rats after CPR compared to MH alone. Capsaicin improved the spontaneous breathing rate and survival rate of Wistar rats after CPR. Conclusions MH may protect cardiac function by mitigating cardiomyocyte necroptosis through regulating TRPV1.

Astrocytes are abundant glial cells in the central nervous system (CNS) that play important roles in brain injury following cardiac arrest (CA). Following brain ischemia, astrocytes trigger endogenous neuroprotective mechanisms, such as fatty acid transport. Lipid droplets (LDs) are cellular structures involved in neutral lipid storage and play essential roles in many biological processes. However, whether lipid droplet metabolism is related to the neurological prognosis after CA remains unclear. JZL-184 is a selective irreversible inhibitor of monoacylglycerol lipase (MAGL), and previous investigations revealed that JZL-184 confers neuroprotection in the brain following stroke. However, further investigations are warranted to explore the effect and mechanism of JZL-184 after CA. Here, we reveal that JZL-184 is neuroprotective after cardiac arrest, as it alleviates astroglial activation by upregulating the expression of transforming growth factor beta 1 (TGF-β1), promotes the transfer of mitochondria from astrocytes to neurons in the astrocyte‒neuron coculture system, and reduces lipid droplet accumulation in neurons. Mechanistically, this protective effect depends on the downstream genes DUSP4 and Rab27b. This study provides additional insights into strategies for inhibiting neurological impairment and suggests a potential therapeutic target after cardiac arrest.

Background Adverse left ventricular remodeling after myocardial infarction (MI) compromises cardiac function and increases heart failure risk. Until now, comprehension of the role transcription factor EB (TFEB) plays after MI is limited. Objectives The purpose of this study was to describe the effects of TFEB on fibroblasts differentiation and extracellular matrix expression after MI. Methods AAV9 (adeno-associated virus) mediated up- and down-regulated TFEB expressions were generated in C57BL/6 mice two weeks before the MI modeling. Echocardiography, Masson, Sirius red staining immunofluorescence, and wheat germ agglutinin staining were performed at 3 days, and 1, 2, and 4 weeks after MI modeling. Fibroblasts collected from SD neonatal rats were transfected by adenovirus and siRNA, and cell counting kit-8 (CCK8), immunofluorescence, wound healing and Transwell assay were conducted. Myocardial fibrosis-related proteins were identified by Western blot. PNU-74654 (100 ng/mL) was used for 12 hours to inhibit β-catenin-TCF/LEF1 complex. Results The up-regulation of TFEB resulted in reduced fibroblasts proliferation and its differentiation into myofibroblasts in vitro studies. A significant up-regulation of EF and down-regulation of myocyte area was shown in the AAV9-TFEB group. Meanwhile, decreased protein level of α-SMA and collagen I were observed in vitro study. TFEB didn’t affect the concentration of β-catenin. Inhibition of TFEB, which promoted cell migration, proliferation and collagen I expression, was counteracted by PNU-74654. Conclusions TFEB demonstrated potential in restraining fibrosis after MI by inhibiting the Wnt/β-catenin signaling pathway.

Hypothermia preconditioning (HPC) improves cardiac function after cardiac arrest, yet the mechanism is unclear. We hypothesized that HPC-activated adenosine monophosphate-activated protein kinase (AMPK) activity may be involved. Adult male Wistar rats were randomly divided into normothermia Control, HPC (cooling to 32–34°C for 30 min), and HPC + Compound C (Compound C 10 mg/kg was injected intraperitoneally 30 min before HPC group). The rats underwent 7 min of untreated ventricular fibrillation (VF) followed by cardiopulmonary resuscitation (CPR). Cardiac function and hemodynamic parameters were evaluated at 4 h after return of spontaneous circulation (ROSC). Survival status was determined 72 h after ROSC. Mechanistically, we further examined the AMPK-Unc-51 Like Autophagy Activating Kinase 1 (ULK1)-mitophagy pathway and autophagic flux in vivo and in vitro. Six of twelve rats in the Control group, 10 of 12 rats in the HPC group, and 7 of 12 rats in HPC + Compound C group were successfully resuscitated. The 72-h survival rates were 1 of 12 Control, 6 of 12 HPC, and 2 of 12 HPC + Compound C rats, respectively ( P = 0.043). Rats in the HPC group demonstrated greater cardiac contractility and hemodynamic stability which were compromised by Compound C. Furthermore, HPC increased the protein levels of p-AMPKα and p-ULK1 and promoted the expression of mitochondrial autophagy-related genes. Compound C decreased the expression of mitochondrial autophagy-related genes and reduced autophagic flux. Consistent with the observations obtained in vivo, in vitro experiments in cultured neonatal rat cardiomyocytes (CMs) demonstrated that HPC attenuated simulated ischemia–reperfusion-induced CM death, accompanied by increased AMPK-ULK1-mitophagy pathway activity. These findings suggest that AMPK-ULK1-mitophagy pathway was activated by HPC and has a crucial role in cardioprotection during cardiac arrest. Manipulation of mitophagy by hypothermia may merit further investigation as a novel strategy to prevent cardiac ischemia–reperfusion injury.

Substantial morbidity and mortality are associated with postcardiac arrest brain injury (PCABI). MicroRNAs(miRNAs) are essential regulators of neuronal metabolism processes and have been shown to contribute to alleviated neurological injury after cardiac arrest. In this study, we identified miRNAs related to the prognosis of patients with neurological dysfunction after cardiopulmonary resuscitation based on data obtained from the Gene Expression Omnibus (GEO) database. Then, we explored the effects of miR-483-5p on mitochondrial biogenesis, mitochondrial-dependent apoptosis, and oxidative stress levels after ischemia‒reperfusion injury in vitro and in vivo. MiR-483-5p was downregulated in PC12 cells and hippocampal samples compared with that in normal group cells and hippocampi. Overexpression of miR-483-5p increased the viability of PC12 cells after ischemia‒reperfusion injury and reduced the proportion of dead cells. A western blot analysis showed that miR-483-5p increased the protein expression of PCG-1, NRF1, and TFAM and reduced the protein expression of Bax and cleaved caspase 3, inhibiting the release of cytochrome c from mitochondria and alleviating oxidative stress injury by inhibiting the production of ROS and reducing MDA activity. We confirmed that miR-483-5p targeted TNFSF8 to regulate the AMPK/JNK pathway, thereby playing a neuroprotective role after cardiopulmonary resuscitation. Hence, this study provides further insights into strategies for inhibiting neurological impairment after cardiopulmonary resuscitation and suggests a potential therapeutic target for PCABI.

The purpose of this cross-sectional survey study is to quantitatively examine the differences in patient trust towards physicians between four different clinical departments in a Chinese hospital. Using a validated modified Chinese version of the Wake Forest Physician Trust Scale, we measured patient trust in each department, and also collected data on patient demographics. A total of 436 patients or family members were surveyed in the departments of emergency medicine, pediatrics, cardiology, and orthopedic surgery. Significant differences were found between the departments, especially between pediatrics (trust score 43.23, range 11-50) and emergency medicine and cardiology (trust scores 45.29 and 45.79, respectively with range of 11-50). The average total score across all four departments was 44.72. There are indications that specifically comparing departments, such as patient demographics or department structure, could be helpful in tailoring patient care to improve physician-patient relationships.

BACKGROUND:Automated detection of return of spontaneous circulation (ROSC) is still an unsolved problem during cardiac arrest. Current guidelines recommend the use of capnography, but most automatic methods are based on the analysis of the ECG and thoracic impedance (TI) signals. This study analysed the added value of EtCO2 for discriminating pulsed (PR) and pulseless (PEA) rhythms and its potential to detect ROSC. MATERIALS AND METHODS:A total of 426 out-of-hospital cardiac arrest cases, 117 with ROSC and 309 without ROSC, were analysed. First, EtCO2 values were compared for ROSC and no ROSC cases. Second, 5098 artefact free 3-s long segments were automatically extracted and labelled as PR (3639) or PEA (1459) using the instant of ROSC annotated by the clinician on scene as gold standard. Machine learning classifiers were designed using features obtained from the ECG, TI and the EtCO2 value. Third, the cases were retrospectively analysed using the classifier to discriminate cases with and without ROSC. RESULTS:EtCO2 values increased significantly from 41 mmHg 3-min before ROSC to 57 mmHg 1-min after ROSC, and EtCO2 was significantly larger for PR than for PEA, 46 mmHg/20 mmHg (p < 0.05). Adding EtCO2 to the machine learning models increased their area under the curve (AUC) by over 2 percentage points. The combination of ECG, TI and EtCO2 had an AUC for the detection of pulse of 0.92. Finally, the retrospective analysis showed a sensitivity and specificity of 96.6% and 94.5% for the detection of ROSC and no-ROSC cases, respectively. CONCLUSION:Adding EtCO2 improves the performance of automatic algorithms for pulse detection based on ECG and TI. These algorithms can be used to identify pulse on site, and to retrospectively identify cases with ROSC.

Objective To investigate the characteristics of myocardial injury and its underlying mechanism in rats resuscitated from cardiac arrest. Methods Forty-two male Wistar rats were randomly(random number) assigned into the post-resuscitation (PR) 4 h, PR 24 h, PR 48 h, and sham groups. Ventricular fibrillation was induced by transcutaneous electrical epicardium stimulation and untreated for 6 min, followed by cardiopulmonary resuscitation (CPR). Myocardial function, glucose metabolism, myocardial ultrastructure, the status of mitochondrial permeability transition pore (MPTP) and mitochondrial membrane potential (MMP) were evaluated at different time points. Results Myocardial dysfunction was found at 4 h after restoration of spontaneous circulation (ROSC). The ejection fraction and cardiac output were decreased (all P<0.01), the diastole left ventricular posterior wall became thicker (P<0.01), and the end-diastolic volume was reduced (P<0.05). However, cardiac function was recovered almost completely at 48 h after ROSC. The PR 4 h group had a higher SUVmax, a more obvious decreased absorbance, and a lower MMP than the sham group (all P<0.01), but no statistically significant differences were noted between the PR 48 h group and the sham group (P>0.05). At 4 h and 24 h after ROSC, the mitochondria was swollen and the mitochondrial crista was sparse, but the myocardial ultrastructure was complete. Conclusions Post resuscitation myocardial dysfunction occurs after ROSC and the myocardial dysfunction is completely reversible at 48 h after ROSC, which may be related to the reversibility of myocardial injury and the gradual recovery of mitochondrial structure and function.

This study investigated the effects of hypothermia induced before cardiac arrest or after return of spontaneous circulation (ROSC) on cardiac function and myocardial mitochondrial injury after ROSC in a rat cardiac arrest model. Sixty healthy, male Wistar rats were randomly divided into the Normothermia group, pre-arrest hypothermia (Pre-HT) group, and post-resuscitation hypothermia (Post-HT) group. The rats underwent 8 min of untreated ventricular fibrillation followed by cardiopulmonary resuscitation. Twelve rats in each group were used to evaluate the left ventricular ejection fraction before ventricular fibrillation and 4 h after ROSC. Survival was determined at 24 h after ROSC. The remaining eight rats in each group were used to detect for heart malondialdehyde, reduced glutathione, adenosine triphosphate levels and mitochondrial histology. Oxygen consumption rate and mitochondrial membrane potential were evaluated 4 h after ROSC; 10 of 12 rats in Pre-HT group, 5 of 12 in Post-HT group, and 6 of 12 in normothermia group were successfully resuscitated. The survival rate of each group was 66.7%, 33.3%, and 25%, respectively. Rats in the Pre-HT group showed less alteration of the mitochondrial ultrastructure and oxidative stress injury, better maintenance of adenine nucleotides, and more preservation of the mitochondrial membrane potential and respiratory function when compared with rats in the Post-HT and normothermia groups. Transient hypothermia is an effective preconditioning stimulus to induce ischemic tolerance in a cardiac arrest model and worthy of further evaluation for potential clinical use. Impact statement In this paper, we investigated the effects of hypothermia induced before ischemia or after ROSC on cardiac function, oxidative stress damage, and myocardial mitochondrial ischemia–reperfusion injury after cardiac arrest in a rat model with VF. We demonstrated that pre-arrest hypothermia conferred greater cardio-protective benefits than delayed post-resuscitation hypothermia, reduced the number of defibrillations required and dosages of epinephrine during CPR, decreased oxidative stress, ameliorated mitochondrial dysfunction, and subsequently improved survival rate.

Mild hypothermia treatment (MHT) improves the neurological function of cardiac arrest (CA) patients, but the exact mechanisms of recovery remain unclear. Herein, we generated a CA and cardiopulmonary resuscitation (CPR) mouse model to elucidate such function. Naïve mice were randomly divided into two groups, a normothemia (NT) group, in which animals had normal body temperature, and a MHT group, in which animals had a body temperature of 33 °C (range: 32–34 °C), after the return of spontaneous circulation (ROSC), followed by CA/CPR. MHT significantly improved the survival rate of CA/CPR mice compared with NT. Mechanistically, MHT increased the expression of Silent Information Regulator 1 (Sirt1) and decreased P53 phosphorylation (p-P53) in the cortex of CA/CPR mice, which coincided with the elevated autophagic flux. However, Sirt1 deletion compromised the neuroprotection offered by MHT, indicating that Sirt1 plays an important role. Consistent with the observations obtained from in vivo work, our in vitro study utilizing cultured neurons subjected to oxygen/glucose deprivation and reperfusion (OGD/R) also indicated that Sirt1 knockdown increased OGD/R-induced neuron necrosis and apoptosis, which was accompanied by decreased autophagic flux and increased p-P53. However, the depletion of P53 did not suppress neuron death, suggesting that P53 was not critically involved in MHT-induced neuroprotection. In contrast, the application of autophagic inhibitor 3-methyladenine attenuated MHT-improved neuron survival after OGD/R, further demonstrating that increased autophagic flux significantly contributes to MHT-linked neuroprotection of CA/CRP mice. Our findings indicate that MHT improves neurological outcome of mice after CA/CPR through Sirt1-mediated activation of autophagic flux.

Aim of study: To determine the association between bioimpedence-detected ventilation and out-of-hospital cardiac arrest (OHCA) outcomes. Methods: This is a retrospective, observational study of 560 OHCA patients from the Dallas-Fort Worth site enrolled in the Resuscitation Outcomes Consortium Trial of Continuous or Interrupted Chest Compressions During CPR from 4/2012 to 7/2015. We measured bioimpedance ventilation (lung inflation) waveforms in the pause between chest compression segments (Physio-Control LIFEPAK 12 and 15, Redmond, WA) recorded through defibrillation pads. We included cases >= 18 years with presumed cardiac cause of arrest assigned to interrupted 30:2 chest compressions with bag-valve-mask ventilation and >= 2 min of recorded cardiopulmonary resuscitation. We compared outcomes in two a priori pre-specified groups: patients with ventilation waveforms in <50% of pauses (Group 1) versus those with waveforms in >= 50% of pauses (Group 2). Results: Mean duration of 30: 2 CPR was 13 +/- 7 min with a total of 7762 pauses in chest compressions. Group 1 (N = 424) had a median 11 pauses and 3 ventilations per patient vs. Group 2 (N = 136) with a median 12 pauses and 8 ventilations per patient, which was associated with improved return of spontaneous circulation (ROSC) at any time (35% vs. 23%, p < 0.005), prehospital ROSC (19.8% vs. 8.7%, p < 0.0009), emergency department ROSC (33% vs. 21%, p < 0.005), and survival to hospital discharge (10.3% vs. 4.0%, p = 0.008). Conclusions: This novel study shows that ventilation with lung inflation occurs infrequently during 30:2 CPR. Ventilation in >= 50% of pauses was associated with significantly improved rates of ROSC and survival.

AIM: To investigate whether neural stem cell-derived exosomes promote the viability and inhibit the apoptosis of neurons under cobalt chloride(CoCl2)-induced hypoxia in vitro.METHODS:The exosomes were isolated based on ultracentrifugation.The exosomal markers,ALG-2-interacting protein X(Alix)and tumor susceptibility gene 101 (TSG101)were identified by Western blot.The shape of exosomes was observed under transmission electron microscope (TEM).The size distributions of exosomes were analyzed by nanoparticle analysis(qNano).The neurons were exposed in CoCl2at different doses(200~600 μmol/L)for 24 h.The exosomes were co-cultured with the neurons pre-treated with CoCl2.The viability and apoptosis of the neurons were measured by CCK-8 assay and TUNEL method.RESULTS: The exosomes released from the neural stem cells expressed exosomal markers Alix and TSG 101.They also displayed a cup-shaped appearance observed under TEM and their sizes were(95.0 ±23.5)nm(n=370).The neuronal viability was sig-nificantly inhibited by CoCl 2in a dose-dependent manner(P<0.05).After treatment with exosomes,the viability of the neuron pre-treated with CoCl2was increased and the apoptotic rate was decreased(P<0.05).CONCLUSION: Neural stem cell-derived exosomes promote the viability and inhibit the apoptosis of rat neurons uneder hypoxia.

Objective To determine the relationship between brain injury and cerebral glucose metabolism in rat model of cardiac arrest. Methods Asphyxia-induced cardiac arrest model was established. Forty-two male Wistar rats were randomly assigned to sham or experimental groups. Rats in the CA4,CA6 and CA8 group were treated with cardiopulmonary resuscitation(CPR) 4 min, 6 min and 8 min after cardiac arrest, respectively. The maximum standardized uptake value (SUVmax) of glucose was detected by PET, and neural defi cit score (NDS) were evaluated at 24 h and 72 h after ROSC. The numbers of injured neurons and apoptotic cells and the protein level of hexokinase I (HXK I) were measured at 72 h after ROSC. Results SUVmax, NDS and the level of HXK I were all decreased after ROSC, and interestingly, this declination of these markers was correlated with the prolongation of the duration of CA, the longer duration of CA the more declination of these biomarkers. Accordingly, the number of injured neurons and apoptotic cells increased were correlated with duration of CA, and thus CA8 group had greater numbers of those cells than CA6 group and CA4 group (P<0.05),and CA6 group had greater numbers of those cells than CA4 group(P<0.05). In addition, the SUVmaxwas positively correlated with NDS(P<0.05), and negatively correlated with the numbers of injured neurons and apoptotic index(P<0.05). Conclusions The degree of brain injury is associated with cerebral glucose metabolism, and PET may become a novel method to assess the severity of brain damage after CA.

Background: Devices that measure ventilation in the pre-hospital setting are deficient especially during early cardiopulmonary resuscitation (CPR) before placement of an advanced airway. Consequently, evidence is limited regarding the role of ventilation during early CPR and its effect on outcomes. Objective: To develop software that automatically identifies ventilation waveforms recorded by defibrillators based on changes in transthoracic impedance during standard CPR. Methods: This was an observational, retrospective analysis of non-traumatic pre-hospital cardiac arrest patients who received 30:2 CPR by emergency medical service rescuers. Data was collected from 550 cases recorded by the bioimpedance channel of defibrillators. Two expert clinicians independently assessed all episodes from the time of initial CPR until placement of an advanced airway, defined acceptable ventilation waveforms, and annotated the pauses between compressions with ventilation waveforms. We then developed software that incorporated the expert criteria and automatically annotated pauses with acceptable ventilations. Results: A total of 7396 pauses were analyzed, mean(SD) duration of 30:2 CPR was 13 (8) min, with 13 (10) pauses/patient, and mean pause duration of 6 (3) s. Reviewer 1 and reviewer 2 identified 2375 and 2249 pauses with any acceptable ventilation, respectively, with an inter-rater reliability of 0.94. The novel software program reproduced expert annotation with excellent agreement ( > 0.8) and high accuracy, both sensitivity and specificity above 90%, compared to two reviewers. The software presented a substantial agreement with the reviewers (kappa > 0.73) for ventilation counts in the pauses. Conclusion: We developed a novel and reliable strategy that enables investigation of ventilation quality during standard CPR using thoracic bioimpedance. This strategy would allow a timely and reliable automatic annotation of large scale resuscitation datasets.

Objective In this study,we hypothesized that anesthetic post-conditioning with sevoflurane at the initiation of cardio-pulmonary resuscitation (CPR) will attenuate cerebral injuries in the model of cardiac arrest.Methods The cardiac arrest model was established through asphyxia.Forty male Wistar rats were assigned to two groups randomly.Rats in the sevoflurane (anesthetic post-conditioning,APoC) group inhaled 1 MAC of sevoflurane during CPR.Rats in the control (CON) group did not receive inhaled sevoflurane during CPR.After return of spontaneous circulation (ROSC),the mean arterial pressure (MAP) and heart rate (HR) was recorded.Before cardiac arrest (baseline) as well as ROSC 1 h and ROSC 4 h,cardiac function was measured.Neurologic deficit scores (NDS) was assessed at 24 and 72 hours after ROSC.At 72 hours after ROSC,coronal brain sections were analyzed by counting TUNEL positive (i.e,apoptotic) cells and Nissl positive (i.e,viable) cells.Results There was no statistical difference in MAP and HR between the two groups.Rats in the APoC group had a thinner LVPW (P ＜ 0.05) and a higher EDV (P ＜ 0.01) compared to the CON group.The apoptotic cells were less and the viable neurons were more in the APoC group compared with CON group (P ＜ 0.05).The NDS was higher in the APoC group at ROSC 24 h and ROSC 72 h (P ＜ 0.05).Conclusion Volatile anesthetic sevoflurane,when administered at initiation of CPR,improves NDS associated with reducing neuronal damage.