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Primary vasopressor efficacy of epinephrine during cardiopulmonary resuscitation (CPR) is due to its α-adrenergic effects. However, epinephrine plays β1-adrenergic actions, which increasing myocardial oxygen consumption may lead to refractory ventricular fibrillation (VF) and poor outcome. Effects of a single dose of esmolol in addition to epinephrine during CPR were investigated in a porcine model of VF with an underlying acute myocardial infarction. VF was ischemically induced in 16 pigs and left untreated for 12 min. During CPR, animals were randomized to receive epinephrine (30 µg/kg) with either esmolol (0.5 mg/kg) or saline (control). Pigs were then observed up to 96 h. Coronary perfusion pressure increased during CPR in the esmolol group compared to control (47 ± 21 vs. 24 ± 10 mmHg at min 5, p < 0.05). In both groups, 7 animals were successfully resuscitated and 4 survived up to 96 h. No significant differences were observed between groups in the total number of defibrillations delivered prior to final resuscitation. Brain histology demonstrated reductions in cortical neuronal degeneration/necrosis (score 0.3 ± 0.5 vs. 1.3 ± 0.5, p < 0.05) and hippocampal microglial activation (6 ± 3 vs. 22 ± 4%, p < 0.01) in the esmolol group compared to control. Lower circulating levels of neuron specific enolase were measured in esmolol animals compared to controls (2[1–3] vs. 21[16–52] ng/mL, p < 0.01). In this preclinical model, β1-blockade during CPR did not facilitate VF termination but provided neuroprotection. [ABSTRACT FROM AUTHOR]

Abstract: Circulatory failure following cardiac arrest (CA) requires catecholamine support and occasionally veno‐arterial extracorporeal membrane oxygenation (vaECMO). VaECMO‐generated blood flow is continuous and retrograde, increasing ventricular stroke work. Our aim was to assess the benefit of a device generating a pulsatile vaECMO flow synchronized with the heart rhythm lowering systolic vaECMO output on the left ventricular ejection fraction (LVEF) and pulmonary capillary pressure (Pcap) after CA. This experimental randomized study in pigs compared standard nonpulsatile vaECMO (control) with pulsatile synchronized vaECMO (study) group using a pulsatility‐generating device. After sedation and intubation, ventricular fibrillation was induced by pacing. After 10‐min ventricular fibrillation, cardiopulmonary resuscitation was performed for 20 min then vaECMO, defibrillation and 0.15 µg/kg/min intravenous epinephrine infusion were initiated. Hemodynamics, Pcap, LVEF by echocardiography and angiography were measured at baseline and every 30 min after the vaECMO start until vaECMO and epinephrine were stopped (at 120 min), and 30 min later. Baseline hemodynamics did not differ between groups; 120 min after vaECMO initiation, LVEF by echocardiography and angiography was significantly higher in the study than control group 55 ± 19% versus 34 ± 13% (P = 0.042), 50 ± 16% versus 33 ± 12% (P = 0.043), respectively. Pcap decreased from baseline by 4.2 ± 8.6 mm Hg in the study group but increased by 5.6 ± 5.9 mm Hg in the control group (P = 0.043). Thirty minutes later, LVEF remained higher in the study group 44 ± 7% versus 26 ± 11% (P = 0.008) while Pcap did not differ. A synchronized pulsatile device decreasing systolic output from vaECMO improved LVEF and Pcap in a pig model of CA and resuscitation. [ABSTRACT FROM AUTHOR]

Aims: Chest compressions (CC) during cardiopulmonary resuscitation are not sufficiently effective in many circumstances. Mechanical CC could be more effective than manual CC, but there are no studies comparing both techniques in children. The objective of this study was to compare the effectiveness of manual and mechanical chest compressions with Thumper device in a pediatric cardiac arrest animal model. Material and methods: An experimental model of asphyxial cardiac arrest (CA) in 50 piglets (mean weight 9.6 kg) was used. Animals were randomized to receive either manual CC or mechanical CC using a pediatric piston chest compressions device (Life-Stat®, Michigan Instruments). Mean arterial pressure (MAP), arterial blood gases and end-tidal CO2 (etCO2) values were measured at 3, 9, 18 and 24 minutes after the beginning of resuscitation. Results: There were no significant differences in MAP, DAP, arterial blood gases and etCO2 between chest compression techniques during CPR. Survival rate was higher in the manual CC (15 of 30 = 50%) than in the mechanical CC group (3 of 20 = 15%) p = 0.016. In the mechanical CC group there was a non significant higher incidence of haemorrhage through the endotracheal tube (45% vs 20%, p = 0.114). Conclusions: In a pediatric animal model of cardiac arrest, mechanical piston chest compressions produced lower survival rates than manual chest compressions, without any differences in hemodynamic and respiratory parameters. [ABSTRACT FROM AUTHOR]

Objectives: High-dose valproic acid in combination with hypothermic-targeted temperature management has been reported to synergistically improve neurologic outcomes after cardiac arrest. This study investigated the potential synergistic mechanisms.Design: Prospective, randomized, experimental study.Setting: University research institution.Subjects: Male Long Evans rats.Intervention: Rats resuscitated from asphyxial cardiac arrest were randomized to one of the three groups: normothermic-targeted temperature management (37°C ± 1°C), hypothermic-targeted temperature management (33° ± 1° × 24 hr + placebo infusion), hypothermic-targeted temperature management plus high-dose valproic acid (300 mg/kg IV × 1 initiated 5 min post return of spontaneous circulation and infused over 20 min) (hypothermic-targeted temperature management + valproic acid).Measurements and Main Results: Seventy-two-hour survival was significantly greater with hypothermic-targeted temperature management + valproic acid, compared to hypothermic-targeted temperature management and normothermic-targeted temperature management (p < 0.05). Survival with good neurologic function, neurodegeneration, expression of HSP70, phosphorylation of Akt and Erk1/2 were not significantly different between hypothermic-targeted temperature management and hypothermic-targeted temperature management + valproic acid. The prevalence of seizures during the first 72-hour postcardiac arrest was significantly lower with hypothermic-targeted temperature management + valproic acid compared to hypothermic-targeted temperature management and normothermic-targeted temperature management (p = 0.01).Conclusions: High-dose valproic acid combined with hypothermic-targeted temperature management prevents postcardiac arrest seizures and improves survival. It remains to be determined if the mechanism of seizure prevention is through the antiepileptic effect of valproic acid or direct neuroprotection. Overall, the combination of high-dose valproic acid and hypothermic-targeted temperature management remains a promising strategy to improve cardiac arrest outcomes. [ABSTRACT FROM AUTHOR]

Background: Standard cardiopulmonary resuscitation (CPR) is ineffective in treating traumatic cardiac arrest (TCA) following hemorrhagic shock despite fluid resuscitation. CPR adjuncts, including abdominal compressions and external counter pressure, have shown some success in laboratory settings. The Abdominal Aortic and Junctional Tourniquet (AAJT) is a device that occludes both venous and arterial blood at the level of the aortic bifurcation and likely increases thoracic pressure when applied to the abdomen. We developed a swine model of controlled hemorrhage to induce a state of TCA to test the ability of the AAJT to improve the efficacy of CPR.Methods: Twelve splenectomized, Yorkshire, male swine (70-90 kg) were randomized into two groups: presence or absence of AAJT placement. Controlled hemorrhage was performed at a rate of 2 mL/kg/min until systolic blood pressure reached below 10 mm Hg (defined as cardiac arrest). Following 3 minutes of arrest, the animals underwent CPR using a mechanical compression device along with either the presence or absence of the AAJT. Concurrently, 5 units of whole blood (2,500 mL) were delivered through the jugular vein at 500 mL/min. Efficacy of CPR was assessed by analyzing rates of return of spontaneous circulation (ROSC) and survival. Blood pressure, carotid blood flow, and other hemodynamic values were also compared.Findings: No significant differences between groups were observed before treatments. The controlled hemorrhage resulted in an average loss of 2,654 ± 323 g of blood over 18.2 ± 3.9 minutes. All animals that had a ROSC survived to the end of the 1-hour observation period. Animals with AAJT survived 83% (5/6) compared to 17% (1/6) of animals without AAJT. Finally, blood pressure, carotid flow, mean pulmonary artery pressure, and end tidal carbon dioxide were all significantly different between groups at the end of the first 10-minute compression period.Discussion/impact/recommendations: These results suggest that the AAJT could allow for increased CPR efficacy in cases of TCA when used in conjunction with rapid, massive blood transfusions. [ABSTRACT FROM AUTHOR]

OBJECTIVES: This study tested the hypothesis that remote perconditioning offers effective and synergistic cardioprotection to terminal warm blood cardioplegia for prompt ventricular recovery after prolonged cardioplegic arrest in an in vivo piglet model. METHODS: Twenty-four piglets were subjected to 120 min of single-dose cardioplegic arrest and were divided into 4 groups according to the mode of reperfusion: control (simple aortic unclamp), remote perconditioning, terminal warm blood cardioplegia or remote perconditioning + terminal warm blood cardioplegia; remote perconditioning (4 cycles of 5-min ischaemia-reperfusion of the lower limb) was applied prior to aortic unclamping. Left ventricular systolic and diastolic functions were assessed by pressure--volume loop analysis at baseline and after 60 min of reperfusion. Biochemical injury was evaluated by plasma troponin T level. RESULTS: The control group showed decreased end-systolic elastance, preload recruitable stroke work and inverse of end-diastolic pressure--volume relationship of 51.3 ± 14.0%, 46.1 ± 22.5% and 34.8 ± 14.9%, respectively. Percentage recovery of end-systolic elastance and preload recruitable stroke work were significantly better with terminal warm blood cardioplegia (with or without remote perconditioning) (end-systolic elastance: 95% confidence interval, 38.6-84.1; preload recruitable stroke work: 95% confidence interval, 0.4-54.3). Percentage recovery of inverse of end-diastolic pressure--volume relationship was significantly better in the remote perconditioning groups (with or without terminal warm blood cardioplegia) (95% confidence interval, 1.6-41.6). No synergistic effects of remote perconditioning and terminal warm blood cardioplegia on troponin T release were noted. CONCLUSIONS: Remote perconditioning offers promising synergistic cardioprotection to terminal warm blood cardioplegia, implicating potential clinical benefit by contributing to prompt left ventricular functional recovery during paediatric open-heart surgery. [ABSTRACT FROM AUTHOR]

Aim Of the Study: Animal models are widely used in cardiac arrest research. This systematic review aimed to provide an overview of contemporary animal models of cardiac arrest.Methods: Using a comprehensive research strategy, we searched PubMed and EMBASE from March 8, 2011 to March 8, 2016 for cardiac arrest animal models. Two investigators reviewed titles and abstracts for full text inclusion from which data were extracted according to pre-defined definitions.Results: Search criteria yielded 1741 unique titles and abstracts of which 490 full articles were included. The most common animals used were pigs (52%) followed by rats (35%) and mice (6%). Studies favored males (52%) over females (16%); 17% of studies included both sexes, while 14% omitted to report on sex. The most common methods for induction of cardiac arrest were either electrically-induced ventricular fibrillation (54%), asphyxia (25%), or potassium (8%). The median no-flow time was 8min (quartiles: 5, 8, range: 0-37min). The majority of studies used adrenaline during resuscitation (64%), while bicarbonate (17%), vasopressin (8%) and other drugs were used less prevalently. In 53% of the studies, the post-cardiac arrest observation time was ≥24h. Neurological function was an outcome in 48% of studies while 43% included assessment of a cardiac outcome.Conclusions: Multiple animal models of cardiac arrest exist. The great heterogeneity of these models along with great variability in definitions and reporting make comparisons between studies difficult. There is a need for standardization of animal cardiac arrest research and reporting. [ABSTRACT FROM AUTHOR]

The purpose of this current study was to evaluate whether improvement of mitochondrial dysfunction was involved in the therapeutic effect of sevoflurane post-conditioning in global cerebral ischemia after cardiac arrest (CA) via the PI3K/Akt pathway. In the first experiment, animals were randomly divided into three groups: a sham group, a CA group, a CA+sevoflurane post-conditioning group (CA+SE). Sevoflurane postconditioning was achieved by administration of 2.5% sevoflurane for 30 min after resuscitation. Sevoflurane post-conditioning has a significant neuroprotective effect by increasing survival rates and reducing neuronal apoptosis. Additionally, the gene and protein expression of PGC-1α, NRF-1, and TFAM, the master regulators of mitochondrial biogenesis, were up-regulated in the CA+SE group, when compared to the CA group. Similarly, in contrast to the CA group, mitochondria-specific antioxidant enzymes, including heat-shock protein 60 (HSP60), peroxiredoxin 3 (Prx3), and thioredoxin 2 (Trx2) were also increased in the CA+SE group. Finally, administration of sevoflurane ameliorated mitochondrial reactive oxygen species (ROS) formation and maintained mitochondrial integrity. In the second experiment, we investigated the relationship between the PI3K/Akt pathway and mitochondrial biogenesis and mitochondriaspecific antioxidant enzymes in sevoflurane-induced neuroprotection. The selective PI3K inhibitor wortmannin not only eliminated the beneficial biochemical processes of sevoflurane by reducing the level of mitochondrial biogenesis-related proteins and aggravating mitochondrial integrity, but also reversed the elevation of mitochondriaspecific antioxidant enzymes induced by sevoflurane. Therefore, our data suggested that sevoflurane post-conditioning provides neuroprotection via improving mitochondrial biogenesis and integrity, as well as increasing mitochondria-specific antioxidant enzymes by a mechanism involving the PI3K/Akt pathway. [ABSTRACT FROM AUTHOR]

Cardiac arrest (CA), if untreated for more than 5 min, can induce severe brain damage, the underlying mechanism of which is still unclear. Previous studies have indicated that high-mobility group box 1 (HMGB1), a nuclear protein implicated in several inflammatory disorders, is involved in the inflammatory processes following brain ischemia. However, the role of HMGB1 in brain dysfunction after CA is yet to be determined. In a rat CA model, HMGB1 protein expression was higher at 1, 3, and 7 days post-CA, compared to that in naïve and sham-treated rats. Following injection of HMGB1 antibody (anti-HMGB1) into the cerebral ventricles, neurological deficit scores were significantly decreased in the CA group as compared to that in the naïve and sham group. Nissl staining showed significant neuronal loss in the hippocampal CA1 region following CA, which was significantly attenuated by anti-HMGB1-treatment (10 and 50 μg) in comparison with the vehicle-injected control. CA induced a significant increase in the levels of the cytokine interleukin-1β (IL-1β) and tumor necrosis factor α (TNF-α) in the hippocampus as revealed by real-time polymerase chain reaction and enzyme-linked immunosorbent assay. Treatment with anti-HMGB1 significantly inhibited IL-1β and TNF-α expression. Our study suggests that HMGB1 contributes significantly to CA-induced brain dysfunction and that inhibiting HMGB1 function and expression may be an effective therapeutic approach to CA-induced ischemic brain injury. [ABSTRACT FROM AUTHOR]

Objective: Ischemic postconditioning (PC) using three intentional pauses at the start of cardiopulmonary resuscitation (CPR) improves outcomes after cardiac arrest in pigs when epinephrine (epi) is used before defibrillation. We hypothesized PC, performed during basic life support (BLS) in the absence of epinephrine, would reduce reperfusion injury and enhance 24h functional recovery.Design: Prospective animal investigation.Setting: Animal laboratorySubjects: Female farm pigs (n=46, 39±1kg).Interventions: Protocol A: After 12min of ventricular fibrillation (VF), 28 pigs were randomized to four groups: (A) Standard CPR (SCPR), (B) active compression-decompression CPR with an impedance threshold device (ACD-ITD), (C) SCPR+PC (SCPR+PC) and (D) ACD-ITD CPR+PC. Protocol B: After 15min of VF, 18 pigs were randomized to ACD-ITD CPR or ACD-ITD+PC. The BLS duration was 2.75min in Protocol A and 5min in Protocol B. Following BLS, up to three shocks were delivered. Without return of spontaneous circulation (ROSC), CPR was resumed and epi (0.5mg) and defibrillation delivered. The primary end point was survival without major adverse events. Hemodynamic parameters and left ventricular ejection fraction (LVEF) were also measured. Data are presented as mean±SEM.Measurements and Main Results: Protocol A: ACD-ITD+PC (group D) improved coronary perfusion pressure after 3min of BLS versus the three other groups (28±6, 35±7, 23±5 and 47±7 for groups A, B, C, D respectively, p=0.05). There were no significant differences in 24h survival between groups.ProtocolB: LVEF 4h post ROSC was significantly higher with ACD-ITD+PC vs ACD-ITD alone (52.5±3% vs. 37.5±6.6%, p=0.045). Survival rates were significantly higher with ACD-ITD+PC vs. ACD-ITD alone (p=0.027).Conclusions: BLS using ACD-ITD+PC reduced post resuscitation cardiac dysfunction and improved functional recovery after prolonged untreated VF in pigs.Protocol Number: 12-11. [ABSTRACT FROM AUTHOR]

Background: Evaluating beneficial effects of potential protective therapies following cardiac arrest in rodent models could be enhanced by exploring behavior and cognitive functions. The Morris Water Maze is a well-known cognitive paradigm to test spatial learning and memory. Results: Behavioral testing with the Morris Water Maze in Sprague-Dawley rats (300 ± 25 g) resuscitated after 8 min of ventricular fibrillation cardiac arrest was carried out 5 and 12 weeks after cardiac arrest (CA) and compared to results of naïve rats (Control). At 5 weeks, within each group latency time to reach the hidden platform (reflecting spatial learning) decreased equally from day 1 to 4 (CA: 105.6 ± 8.2 vs. 8.9 ± 1.2 s, p < 0.001; Control: 75.5 ± 13.2 vs. 17.1 ± 4.5, p < 0.001) with no differences between groups (p = 0.138). In the probe trial 24 h after the last trial, time spent in the target sector (reflecting memory recall) within each group was significantly longer (CA: 25 ± 1.3; Control: 24.7 ± 2.5 s) than in each of the three other sectors (CA: 7.7 ± 0.7, 14.3 ± 2.5, 8.4 ± 0.8 and Control: 7.8 ± 1.2, 11.7 ± 1.5, 10.3 ± 1.6 s) but with no significantly differences between groups. Seven days later (reflecting memory retention), control group animals remained significantly longer in the target sector compared to every other sector, whereas the cardiac arrest group animals did not. Even 12 weeks after cardiac arrest, the single p values showed that the control animals displayed a trend to perform better than the resuscitated animals. Conclusions: Memory recall was impaired early after 8 min of ventricular fibrillation cardiac arrest and might be a more valuable tool for cognitive testing than learning recall after global ischemia due to cardiac arrest. [ABSTRACT FROM AUTHOR]

Introduction: Over the last 40 years omega-3 polyunsaturated fatty acids (PUFAs) have been shown to be anti-arrhythmic or pro-arrhythmic depending on the method and duration of administration and model studied. We previously reported that omega-3 PUFAs do not confer anti-arrhythmic properties and are pro-arrhythmic in canine model of sudden cardiac death (SCD). Here, we evaluated the effects of chronic omega-3 PUFA treatment in post-MI animals susceptible (VF+) or resistant (VF-) to ventricular tachyarrhythmias. Methods: Perforated patch clamp techniques were used to measure cardiomyocyte action potential durations (APD) at 50 and 90% repolarization and short term variability of repolarization. The early repolarizing transient outward potassium current Ito was also studied. Results: Omega-3 PUFAs prolonged the action potential in VF- myocytes at both 50 and 90% repolarization. Short term variability of repolarization was increased in both untreated and treated VF- myocytes vs. controls. Ito was unaffected by omega-3 PUFA treatment. Omega-3 PUFA treatment attenuated the action potential prolongation in VF+ myocytes, but did not return repolarization to control values. Conclusions: Omega-3 PUFAs do not confer anti-arrhythmic properties in the setting of healed myocardial infarction in a canine model of SCD. In canines previously resistant to ventricular fibrillation (VF-), omega-3 PUFA treatment prolonged the action potential in VF- myocytes, and may contribute to pro-arrhythmic responses. [ABSTRACT FROM AUTHOR]

Background: Current research highlights the role of microcirculatory disorders in post-cardiac arrest patients. Affected microcirculation shows not only dissociation from systemic hemodynamics but also strong connection to outcome of these patients. However, only few studies evaluated microcirculation directly during cardiac arrest (CA) and cardiopulmonary resuscitation (CPR). The aim of our experimental study in a porcine model was to describe sublingual microcirculatory changes during CA and CPR using recent videomicroscopic technology and provide a comparison to parameters of global hemodynamics.Methods: Cardiac arrest was induced in 18 female pigs (50 ± 3 kg). After 3 min without treatment, 5 min of mechanical CPR followed. Continuous hemodynamic monitoring including systemic blood pressure and carotid blood flow was performed and blood lactate was measured at the end of baseline and CPR. Sublingual microcirculation was assessed by the Sidestream Dark Field (SDF) technology during baseline, CA and CPR. Following microcirculatory parameters were assessed off-line separately for capillaries (≤20 µm) and other vessels: total and perfused vessel density (TVD, PVD), proportion of perfused vessels (PPV), microvascular flow index (MFI) and heterogeneity index (HI).Results: In comparison to baseline the CA small vessel microcirculation was only partially preserved: TVD 15.64 (13.59-18.48) significantly decreased to 12.51 (10.57-13.98) mm/mm(2), PVD 15.57 (13.56-17.80) to 5.53 (4.17-6.60) mm/mm(2), PPV 99.64 (98.05-100.00) to 38.97 (27.60-46.29) %, MFI 3.00 (3.00-3.08) to 1.29 (1.08-1.58) and HI increased from 0.08 (0.00-0.23) to 1.5 (0.71-2.00), p = 0.0003 for TVD and <0.0001 for others, respectively. Microcirculation during ongoing CPR in small vessels reached 59-85 % of the baseline values: TVD 13.33 (12.11-15.11) mm/mm(2), PVD 9.34 (7.34-11.52) mm/mm(2), PPV 72.34 (54.31-87.87) %, MFI 2.04 (1.58-2.42), HI 0.65 (0.41-1.07). The correlation between microcirculation and global hemodynamic parameters as well as to lactate was only weak to moderate (i.e. Spearman's ρ 0.02-0.51) and after adjustment for multiple correlations it was non-significant.Conclusions: Sublingual microcirculatory parameters did not correlate with global hemodynamic parameters during simulated porcine model of CA and CPR. SDF imaging provides additional information about tissue perfusion in the course of CPR. [ABSTRACT FROM AUTHOR]

Inflammation-dominated sympathetic sprouting adjacent to the necrotic region following myocardial infarction (MI) has been implicated in the etiology of arrhythmias resulting in sudden cardiac death; however, the mechanisms responsible remain to be elucidated. Although being a key immune mediator, the role of Notch has yet to be explored. We investigated whether Notch regulates macrophage responses to inflammation and affects cardiac sympathetic reinnervation in rats undergoing MI. MI was induced by coronary artery ligation. A high level of Notch intracellular domain was observed in the macrophages that infiltrated the infarct area at 3 days post-MI. The administration of the Notch inhibitor N-N-(3,5-difluorophenacetyl-L-alanyl)-S-phenylglycine-t-butyl ester (DAPT) (intravenously 30 min before MI and then daily until death) decreased the number of macrophages and significantly increased the M2 macrophage activation profile in the early stages and attenuated the expression of nerve growth factor (NGF). Eventually, NGF-induced sympathetic hyperinnervation was blunted, as assessed by the immunofluorescence of tyrosine hydroxylase. At 7 days post-MI, the arrhythmia score of programmed electric stimulation in the vehicle-treated infarcted rats was higher than that in rats treated with DAPT. Further deterioration in cardiac function and decreases in the plasma levels of TNF-α and IL-1β were also detected. In vitro studies revealed that LPS/IFN-γ upregulated the surface expression of NGF in M1 macrophages in a Notch-dependent manner. We concluded that Notch inhibition during the acute inflammatory response phase is associated with the downregulation of NGF, probably through a macrophage-dependent pathway, thus preventing the process of sympathetic hyperinnervation. [ABSTRACT FROM AUTHOR]

Background: There are no clear evidence-based recommendations on the use of different techniques of respiratory support and chest compressions (CC) during neonatal cardiopulmonary resuscitation (CPR). Objectives: To determine the effects of different respiratory support strategies along with CC representing clinical practice on the return of spontaneous circulation (ROSC) in hypoxic newborn piglets with cardiac arrest. We hypothesized that use of a T-piece resuscitator (TPR) providing positive end-expiratory pressure (PEEP) reduces time to ROSC as compared to a self-inflating bag (SIB) without PEEP. Furthermore, we explored the effects of a ventilator providing inflations without synchrony to CC. Methods: Thirty-three newborn piglets were exposed to hypoxia until asystole occurred and randomized into three groups and resuscitated according to ILCOR guidelines: group 1 = TPR [peak inspiratory pressure (PIP)/PEEP of 25/5 cm H2O, rate 30/min], inflations interposed between CC (3:1 ratio); group 2 = SIB (PIP of 25 cm H2O without PEEP, rate 30/min), inflations interposed between CC (3:1 ratio), and group 3 = ventilator (PIP/PEEP of 25/5 cm H2O, rate 30/min), CC were applied with a rate of 120/min without synchrony to inflations. Animals were supported for 120 min after ROSC. Primary outcome was time to ROSC. Results: All animals achieved ROSC. We found no significant difference in time to ROSC between groups [median (IQR); TPR: 150 s (150-210); SIB: 150 s (120-180); ventilator: 180 s (150-345)]. There was no difference in use of epinephrine, in blood gases or hemodynamic parameters during the 120-min observation time after ROSC. Conclusions: We found no significant effect of different respiratory support strategies during CPR on ROSC. © 2015 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

Background. The pulmonary donor pool would increase substantially if lungs could be donated after cardiac death (DCD). There have been ethical and legal obstacles since administration of heparin and cooling has to be done immediately after cardiac death. This study examines whether ventilation of DCD lungs without administering heparin or cooling the lungs after cardiac death could improve graft function.Method.Twelve donor pigs with a mean bodyweight of 70 kg were randomized into two groups. Six animals were ventilatedin situwith 50% oxygen, 4 L/min, and 5 cm H2O in positive end-expiratory pressure or PEEP for 2 h after cardiac death. Six animals served as non-ventilated controls and were exposed to warm ischemia for 2 h. After 2 h, all lungs were harvested and flush perfused with Perfadex®solution and stored at 8°C for another 2 h. Anex vivolung perfusion or EVLP circuit was used for evaluation.Results.Non-ventilated lungs developed pulmonary edema, and had highly impaired blood gas levels and a significantly increased weight. The ventilated lungs demonstrated excellent blood gas levels and unchanged weight.Conclusion.The increase in tolerable warm ischemic time in combination with avoiding heparinization and cooling might facilitate the use of DCD lungs for transplantation. [ABSTRACT FROM AUTHOR]

Background: Pulse oximetry is widely used in intensive care and emergency conditions to monitor arterial oxygenation and to guide oxygen therapy. Objective: To study the reliability of pulse oximetry in comparison with CO-oximetry in newborn piglets during cardiopulmonary resuscitation (CPR). Methodology: In a prospective cohort study in 30 healthy newborn piglets, cardiac arrest was induced, and thereafter each piglet received CPR for 20 min. Arterial oxygen saturation was monitored continuously by pulse oximetry (SpO2). Arterial blood was analyzed for functional oxygenation (SaO2) every 2 min. SpO2 was compared with coinciding SaO2 values and bias considered whenever the difference (SpO2 - SaO2) was beyond ±5%. Results: Bias values were decreased at the baseline measurements (mean: 2.5 ± 4.6%) with higher precision and accuracy compared with values across the experiment. Two minutes after cardiac arrest, there was a marked decrease in precision and accuracy as well as an increase in bias up to 13 ± 34%, reaching a maximum of 45.6 ± 28.3% after 10 min over a mean SaO2 range of 29-58%. Conclusion: Pulse oximetry showed increased bias and decreased accuracy and precision during CPR in a model of neonatal cardiac arrest. We recommend further studies to clarify the exact mechanisms of these false readings to improve reliability of pulse oximetry during the marked desaturation and hypoperfusion found during CPR. © 2014 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The article presents recommendations for CPR in veterinary patients. It mentions that some form of hands-on practice is suggested for key skills, such as starting an electrocardiogram (ECG), passing an endotracheal tube and chest compressions. It states that practice policy to confirm resuscitation status is significant where the patient with condition that can predispose to arrest, such as coagulopathies, cardiac failure and sepsis.

Objective: Myocardial reperfusion injury can induce further cardiomyocyte death and contribute to adverse cardiovascular outcomes after myocardial ischemia, cardiac surgery, or circulatory arrest. Exposure to near-infrared (NIR) light at the time of reoxygenation protects neonatal rat cardiomyocytes and HL-1 cells from injury. We hypothesized that application of NIR at 670 nm would protect the heart against ischemia-reperfusion injury. Methods: We assessed the protective role of NIR in in vivo and in vitro rat models of ischemia-reperfusion injury. Results: NIR application had no effect on the function of the nonischemic isolated heart, and had no effect on infarct size when applied during global ischemia. In the in vivo model, NIR commencing immediately before reperfusion decreased infarct size by 40%, 33%, 38%, and 77%, respectively, after regional ischemic periods of 30, 20, 15, and 10 min. Serum cardiac troponin I (cTnI) was significantly reduced in the 15 min group, whereas creatine kinase (CK) and lactate dehydrogenase (LDH) levels were not affected. Conclusions: We have demonstrated the safety of NIR application in an in vitro rat isolated model. In addition, we have demonstrated safety and efficacy when using NIR for cardioprotection in an in vivo rat ischemia model, and that this cardioprotection is dependent upon some factor present in blood, but not in perfusion buffer. Results show potential for cTnI, but not CK or LDH, as a biomarker for cardioprotection by NIR. NIR may have therapeutic utility in providing myocardial protection from ischemia-reperfusion injury. [ABSTRACT FROM AUTHOR]

We investigated the feasibility of OCT in monitoring the viability of the brain. It was confirmed that after an overdose of pentobarbital sodium salt for an euthanasia, the OCT signal intensity increased before cardiac arrest and finally became 2.7 times, and by periodically changing the tissue temperature from 20 to 32 °C in vivo, average correlation coefficients between the ratio of signal intensity (RSI) and temperature were determined to be −0:42 to −0:50. RSI reversibly changed with subsequent variations of temperatures and finally increased rapidly just before cardiac arrest. These results indicate that RSI could correspond to decreases in viability. [ABSTRACT FROM AUTHOR]

Purpose: Some of the neuroprotective effects of hydrogen sulfide (HS) have been attributed to systemic hypometabolism and hypothermia. However, systemic metabolism may vary more dramatically than brain metabolism after cardiac arrest (CA). The authors investigated the effects of inhaled exogenous hydrogen sulfide on brain metabolism and neurological function in rabbits after CA and resuscitation. Methods: Anesthetized rabbits were randomized into a sham group, a sham/HS group, a CA group, and a CA/HS group. Exogenous 80 ppm HS was administered to the sham/HS group and the CA/HS group which suffered 3 min of untreated CA by asphyxia and resuscitation. Effects on brain metabolism (cerebral extraction of oxygen (CEO), arterio-jugular venous difference of glucose [AJVD(glu)] and lactate clearance), S100B, viable neuron counts, neurological dysfunction score, and survival rate were evaluated. Results: CEO, AJVD(glu), and lactate increased significantly after CA. Inhalation of 80 ppm HS significantly increased CEO (25.04 ± 7.11 vs. 16.72 ± 6.12 %) and decreased AJVD(glu) (0.77 ± 0.29 vs. 1.18 ± 0.38 mmol/L) and lactate (5.11 ± 0.43 vs. 6.01 ± 0.64 mmol/L) at 30 min after resuscitation when compared with the CA group (all P < 0.05). In addition, neurologic deficit scores, viable neuron counts, and survival rate were significantly better whereas S100B was decreased after HS inhalation. Conclusions: The present study reveals that inhalation of 80 ppm HS reduced neurohistopathological damage and improves early neurological function after CA and resuscitation in rabbits. The increased CEO and decreased AJVD(glu) and enhanced lactate clearance may be involved in the protective effects. [ABSTRACT FROM AUTHOR]

The aim of this study is to compare cerebral protection using antegrade cerebral perfusion (ACP) with various flow rates during deep hypothermic circulatory arrest (DHCA) in a piglet model. Twenty-three piglets were randomized to five groups: the control group ( n = 3), DHCA group ( n = 5), ACP25 group ( n = 5), ACP50 group ( n = 5), and ACP80 group ( n = 5). Three control piglets did not undergo operations. Twenty piglets underwent cardiopulmonary bypass (CPB) and DHCA for 60 min at 20°C. ACP was conducted at 0, 25, 50, and 80 mL/kg/min in the DHCA, ACP25, ACP50, and ACP80 group, respectively. Serum S-100B protein and neuron-specific enolase were monitored, and brain tissues were assayed for the activities of caspase-3 and stained for the evidence of apoptotic cellular injury. Rise in serum S-100B level (post-CPB-pre-CPB) in the ACP50 group was significantly lower than that in the ACP80 group ( P = 0.001). Caspase-3 levels were significantly elevated in the ACP80 group compared with the ACP25 ( P = 0.041) and ACP50 group ( P = 0.01), while positive terminal deoxyneucleotidyl transferase-mediated biotin-dUTP nick end labeling reaction scores in the ACP80 group were significantly higher than those in the ACP25 ( P = 0.043) and ACP50 group ( P = 0.023). Cerebral protection effects of ACP at 25 and 50 mL/kg/min were superior to that of ACP at 80 mL/kg/min as determined by cerebral markers, immunology, and histology. [ABSTRACT FROM AUTHOR]

Abstract: Objective: To investigate the effects of Shen-Fu injection (SFI) on postresuscitation lung injury in a porcine model of cardiac arrest. Methods: Twenty-four anaesthetised male Landrace pigs were subjected to 4min of untreated ventricular fibrillation (VF), followed by standard cardiopulmonary resuscitation. Sixteen successfully resuscitated pigs were randomised into two groups (eight pigs per group); one group received an SFI infusion and the other group received a normal saline infusion, at an infusion rate of 0.24mg/min from 15min after the return of spontaneous circulation (ROSC) until 6h after ROSC. Results: Oxygenation index, respiratory index, oxygen delivery, oxygen consumption, oxygen extraction, dynamic lung compliance, airway resistance, external vascular lung water index, and pulmonary vascular permeability index at 15min, 30min, 1h, 2h, 4h, and 6h after ROSC were all worse than baseline in the saline group, and were all better in the SFI group than in the saline group. The pulmonary protective effects of SFI were further confirmed by histopathological and ultrastructural observations of lung tissue. SFI infusion resulted in lower apoptosis index, caspase-3 protein expression, and malondialdehyde content of lung tissue after ROSC, and increased Bcl-2 protein expression and superoxide dismutase, Na+-K+-ATPase, and Ca2+-ATPase activity compared with the saline group. Conclusion: Shen-Fu injection can attenuate postresuscitation lung injury through suppression of lung cell apoptosis and improvement of energy metabolism and antioxidant capacity. [Copyright &y& Elsevier]

Abstract: Aim: The nonselective Cannabinoid (CB) receptor agonist, WIN55, 212-2, was demonstrated to induce hypothermia and improve post-resuscitation outcomes in a rat post-cardiac arrest model. The present study was to explore the potential mechanisms of WIN55, 212-2 on thermoregulation following resuscitation and to investigate which class of CB receptors was involved in WIN55, 212-2-induced hypothermia. Methods: Ventricular fibrillation (VF) was induced and untreated for 6min in 20 male Sprague-Dawley rats. Defibrillation was attempted after 8min of Cardiopulmonary resuscitation (CPR). Five min post-resuscitation, resuscitated animals were randomized to receive an intramuscular injection of selective CB1 receptors antagonist, SR141716A (5mgkg−1); selective CB2 receptors antagonist SR144528 (5mgkg−1); or placebo. Thirty min after injection, animals received continuous intravenous infusion of WIN55, 212-2 (1.0mgkg−1 h−1) for 4h while control animals received placebo. The identical temperature environment was maintained in all animals. Results: In animals treated with WIN55, 212-2, blood temperatures decreased progressively from 37°C to 34°C within 4h. This hypothermic effect was completely blocked by CB1 but not CB2 antagonist. Accordingly, significantly better cardiac output, ejection fraction and myocardial performance index, reduced neurological deficit scores, improved microcirculation and longer duration of survival were observed in WIN55, 212-2-treated animals, which were also completely abolished by pretreatment with CB1 antagonist. Conclusions: Pharmacologically induced hypothermia with WIN55, 212-2 improved post-resuscitation myocardial and cerebral function, associated with a significantly increased duration of survival in a rat post-cardiac arrest model. The hypothermic and resulted beneficial effects of WIN55, 212-2 were mediated through CB1 receptors. [Copyright &y& Elsevier]

The article discusses a study which compared the mitochondria function and calcium threshold for triggering of mitochondrial permeability transition pore opening in bupivacaine-induced cardiac arrest before and after resuscitation with lipid emulsion. The study included adult male Sprague-Dawley rats that were given bupivacaine and lipid emulsion. It found that bupivacaine resulted in asystole, while lipid emulsion improved cardiac function.

Abstract: Objective: To study the changes of brain water diffusion and cerebral haemodynamics of cortical areas using magnetic resonance imaging (MRI) in canine models of cardiac arrest (CA) and restoration of spontaneous circulation (ROSC). The secondary study objective was to evaluate whether MRI can be used to observe haemodynamic disorders in brain microcirculation. Methods: CA was induced in six beagle dogs using electrical stimulation followed by resuscitation to spontaneous circulation 3min later. The dogs were scanned using MRI for echo planar, diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI) with injection of Gd-diethylene triamine pentaacetic acid (DTPA) prior to induction of CA and 3 days after ROSC. The arterial blood pressure, unilateral common carotid artery flow and intracranial microcirculation were recorded. Results: All dogs successfully underwent electric-induced ventricular fibrillation which lasted 3min and were resuscitated to maintain blood pressure stability. Serial MRI scans found that cerebral blood flow (RCBF) decreased in day 1 after ROSC and returned to baseline on day 3. Apparent diffusion coefficient (ADC), however, decreased on day 1 and remained lower than baseline on day 3, with 765.8±82.5×10−6 mm2 s−1 on day 1 and 770.4±59.4×10−6 mm2 s−1 on day 3 comparing to 855.8±43.4×10−6 mm2 s−1 on baseline. Conclusions: These data provide the evidence that early MRI can be used to observe acute haemodynamic disorders in brain microcirculation in a canine model of cardiac arrest. [Copyright &y& Elsevier]

The article discusses a study which examined the effect of mild hypothermia on the in vivo pharmacokinetics of fentanyl and midazolam following cardiac arrest. The study concluded that mild hypothermia reduces the systemic clearances of fentanyl and midazolam in rats after cardiac arrest. It also revealed that alterations in cytochrome P450 3a2 metabolic capacity plays a role in how mild hypothermia affect fentanyl and midazolam pharmacokinetics.

1. The effects of amiodarone on ventricular electrophysiological parameters, especially the dispersion of ventricular repolarization, were investigated in a canine model of congestive heart failure (CHF). 2. Dogs were randomized to either a control, amiodarone, CHF, or CHF+amiodarone group. Dogs in the CHF and CHF+amiodarone groups underwent 4–5 weeks of rapid ventricular pacing; dogs in the control and amiodarone groups underwent sham operation only. Amiodarone (20 mg/kg per day) was administered orally, beginning on postoperative Day 1, in the treatment groups; ventricular electrophysiological variables were evaluated 4–5 weeks after rapid pacing or sham operation. 3. In CHF dogs, the transmural dispersion ventricular repolarization time (TDVRT) increased significantly. Amiodarone significantly decreased the TDVRT in CHF dogs. The ventricular fibrillation threshold (VFT) decreased in the CHF group. Amiodarone increased the VFT in CHF dogs. 4. The TDVRT increased in CHF dogs, but amiodarone decreased TDVRT and increased VFT in these dogs. These results suggest a beneficial effect of amiodarone on malignant arrhythmias and may provide the basis for its use in CHF patients. [ABSTRACT FROM AUTHOR]

Aim: Mild hypothermia (MH) after cardiac arrest attenuates hypoxic brain injury and improves survival. As MH increases contractility in normal hearts, we hypothesized that MH improves cardiovascular function after cardiac arrest. Methods: In 16 anaesthetized pigs (64 ± 2 kg), ventricular fibrillation was induced electrically for 5 min. At 10 min after resuscitation and return of spontaneous circulation (ROSC), pigs were assigned to normothermia (NT, 38 °C, n = 8) or MH (33 °C, n = 8, intravascular cooling). Results: At ROSC 6 h vs. baseline, heart rate (HR) was unchanged in NT, but decreased in MH. Cardiac output (CO, l min−1) decreased in MH (3.5 ± 0.2 vs. 5.5 ± 0.4, P < 0.05) more than in NT (4.8 ± 0.4 vs. 5.7 ± 0.4, P = ns). Mixed venous oxygen saturation decreased in NT (56 ± 2 vs. 66 ± 3%, P < 0.05), but remained constant in MH (64 ± 2 vs. 65 ± 2%) due to a 35% decrease of whole body oxygen consumption. Left ventricular (LV) dP/dtmax (mmHg s−1) decreased in NT (1163 ± 97 vs. 1665 ± 134, P < 0.05), but was preserved in MH (1602 ± 102 vs. 1603 ± 96), whereas LV relaxation was profoundly slowed during MH. Pressure-volume analysis confirmed improved LV systolic function during MH, but also demonstrated decreased LV end-diastolic distensibility, which was further potentiated by right atrial pacing at baseline HR. MH did not increase plasma catecholamine levels. Spectral analysis of heart rate variability revealed reduced sympathetic activation during MH. Conclusion: The induction of MH after cardiac resuscitation improves systolic myocardial function without further sympathetic activation. A reduced metabolism during MH outweighs a decreased CO and thereby acts favourably on systemic oxygen supply/demand balance. [ABSTRACT FROM AUTHOR]

Ongoing interest in brain ischemia research has provided data showing that ischemia may be involved in the pathogenesis of Alzheimer disease. Brain ischemia in the rat produces a stereotyped pattern of selective neuronal degeneration, which mimics early Alzheimer disease pathology. The objective of this study was to further develop and characterize cardiac arrest model in rats, which provides practical way to analyze Alzheimer-type neurodegeneration. Rats were made ischemic by cardiac arrest. Blood-brain barrier (BBB) insufficiency, accumulation of different parts of amyloid precursor protein (APP) and platelets inside and outside BBB vessels were investigated in ischemic brain up to 1-year survival. Ischemic brain tissue demonstrated haphazard BBB changes. Toxic fragments of APP deposits were associated with the BBB vessels. Moreover our study revealed platelet aggregates in- and outside BBB vessels. Toxic parts of APP and platelet aggregates correlated very well with BBB permeability. Progressive injury of the ischemic brain parenchyma may be caused not only by a degeneration of neurons destroyed during ischemia but also by chronic damage in BBB. Chronic ischemic BBB insufficiency with accumulation of toxic components of APP in the brain tissue perivascular space, may gradually over a lifetime, progress to brain atrophy and to full blown Alzheimer-type pathology. [ABSTRACT FROM AUTHOR]

The article reports on a study conducted on a male cynomolgus macaque that suffered sudden cardiac arrest during a surgical operation. A background of the case is provided including the discovery of a white firm mass at the base of the heart during necropsy. Differential diagnoses of lymphoma, tuberculosis or mycoses are presented along with the microscopic findings on the mass which consisted of granulomatous lesion. Polymerase chain reaction (PCR) assay to confirm Aspergillus spp is explained together with its results.

Abstract: Background: Intravenous (IV) infusion of ice cold saline is an effective method to initiate induction of mild therapeutic hypothermia (MTH) following resuscitation from out-of-hospital cardiac arrest (OOHCA). Intraosseous (IO) infusion of cold saline may be an alternative method to induce MTH. Objective: The goal of this study was to determine if IO infusion of cold saline is a comparable alternative to IV infusion for inducing MTH in a laboratory swine model of cardiac arrest. Methods: Ten mixed breed swine were resuscitated from cardiac arrest and randomized post-resuscitation to infusion with ice cold saline using either IO (n =5) or IV (n =5) access. The study endpoints were either a goal esophageal temperature of 34°C or the elapse of a 30min time period, simulating a long prehospital transport. Results: Four of five pigs in the IV infusion group achieved goal temperature within 30min compared to 0/5 in the IO infusion group (p =0.048). The mean esophageal temperature change was significantly higher in the IV group when compared to the IO group (p <0.001). Post-arrest hemodynamic parameters were similar between the two groups. Conclusions: IV infusion of ice cold saline is an efficacious method to achieve MTH in this swine model of cardiac arrest. Furthermore, IO infusion of cold saline is not sufficient to induce MTH in the time routinely available in the prehospital setting following OOHCA. [Copyright &y& Elsevier]

Abstract: Aim of the study: In comparison to adrenaline, administration of vasopressin increases adrenal gland perfusion, but decreases catecholamine plasma concentrations when compared to saline placebo. We directly compared the effects of adrenaline with different doses of vasopressin on adrenal gland perfusion, and noradrenaline plasma concentrations during CPR. Methods: Twenty-one pigs received either 0.2mgkg−1 adrenaline (n =7), 0.2Ukg−1 vasopressin (n =7), or 0.8Ukg−1 vasopressin (n =7) after 4min of cardiac arrest and 3min of CPR. Adrenal gland perfusion was determined using radiolabeled microspheres, noradrenaline plasma concentration was measured by high pressure liquid chromatography. Results: Before administration of vasopressor drugs during CPR, adrenal gland perfusion, and noradrenaline plasma concentrations were not different between groups. Ninety seconds and 5min after drug administration, adrenal gland perfusion was significantly higher with both doses of vasopressin when compared with adrenaline, but was not different between the vasopressin groups. Noradrenaline plasma concentrations were 23684±5036pgml−1 with adrenaline, 11455±2450pgml−1 with 0.2Ukg−1 vasopressin, and 12119±2921pgml−1 with 0.8Ukg−1 vasopressin at 90s after administration of vasopressors (p <.05 for both doses of vasopressin vs adrenaline). Five of seven animals in the adrenaline group, five of seven animals in the 0.2Ukg−1 vasopressin group, and six of seven animals in the 0.8Ukg−1 vasopressin group were successfully defibrillated. Conclusions: Vasopressin enhances adrenal gland perfusion, but decreases noradrenaline plasma concentration when compared to adrenaline during CPR. Neither adrenal gland perfusion nor noradrenaline plasma concentration affect survival in this pig model of cardiac arrest. [Copyright &y& Elsevier]

Abstract: Objective: The study investigated a possible neuroprotective potency of minocycline in an experimental asphyxial cardiac arrest (ACA) rat model. Clinically important survival times were evaluated thus broadening common experimental approaches. Methods: Adult rats were subjected to 5min of ACA followed by resuscitation. There were two main treatment groups: ACA and sham operated. Relating to minocycline treatment each group consisted of three sub-groups: pre-, post-, and sans-mino, with three different survival times: 4, 7, and 21 days. Neurodegeneration and microgliosis were monitored by immunohistochemistry. Alterations of microglia-associated gene expression were analyzed by quantitative RT-PCR. Results: ACA induced massive nerve cell loss and activation of microglia/macrophages in hippocampal CA1 cell layer intensifying with survival time. After 7 days, minocycline significantly decreased both, neuronal degeneration and microglia response in dependence on the application pattern; application post ACA was most effective. After 21 days, neuroprotective effects of minocycline were lost. ACA significantly induced expression of the microglia-associated factors Ccl2, CD45, Mac-1, F4-80, and Tnfa. Independent on survival time, minocycline affected these parameters not significantly. Expression of iNOS was unaffected by both, ACA and minocycline. Conclusions: In adult rat hippocampus microglia was significantly activated by ACA. Minocycline positive affected neuronal survival and microglial response temporary, even when applied up to 18h after ACA, thus defining a therapeutically-relevant time window. As ACA-induced neuronal cell death involves acute and delayed events, longer minocycline intervention targeting also secondary injury cascades should manifest neuroprotective potency, a question to be answered by further experiments. [Copyright &y& Elsevier]

Abstract: Aim of the study: A reproducible long-term intensive care and outcome cardiac arrest model for exploring new cerebral preservation strategies is needed. We tried to determine effects and limitations of current therapies after different ‘no-flow’ times. Methods: Thirty-five female Large White Breed pigs (26–37kg) were included in the study. Three pigs served as sham animals without cardiac arrest (CA). Ventricular fibrillation (VF) CA was induced in 32 animals for 0, 7, 10 and 13min (each group consisting of 8 animals), followed by 8min of chest compressions, mechanical ventilation and vasopressors. Thereafter, up to 3 defibrillations were delivered. After restoration of spontaneous circulation (ROSC), the animals underwent intensive care for 20h. Neurologic examination was performed at designated time points using a neurologic deficit (ND) and an overall performance category (OPC) score. Results: Restoration of spontaneous circulation was achieved in 8 of 8 animals in the 0min-group, 6 of 8 in the 7min-group, 7 of 8 in the 10min-group and 0 of 8 in the 13min-group. All animals of the sham-group and 0min-group were neurologically intact survivors; the 7 and 10min-groups showed a median ND of 55%(26;94) and 73%(58;78), respectively. There were no significant differences between the 7 and 10min-groups regarding OPC and NDS. Coronary perfusion pressure during CPR decreased concordantly with ‘no-flow’ times with a tendency towards significance. Conclusion: This study established a reproducible cardiac arrest and resuscitation model in pigs which will be used to test novel resuscitation strategies to improve neurologic outcome after cardiac arrest. [ABSTRACT FROM AUTHOR]

The article presents a study that tests whether cold aortic flush and chest compressions will improve neurologic outcomes after cardiac arrest in pigs, as compared to conventional resuscitation. Twenty- four female pigs were part of the study wherein experimental protocol was approved by the institutional animal investigation committee. It concludes the feasibility of the preservation and resuscitation by deep cerebral hypothermia with chest compressions and improvement of neurologic outcomes.

The article discusses a study which evaluates the impacts of defibrillation delivered during the manual chest compression (CC) on the transthoracic defibrillation threshold (DFT). A randomized, prospective study was performed on porcine model of cardiac arrest to compare the DFT at different phases during manual CC. The findings reveal that the effectiveness of defibrillation is greater when electrical shock is carried out during manual CC's upstroke phase.

Cardiac markers have been used in order to assist clinical diagnosis of animals with heart disease, more accurately, enabling the establishment of earlier prognosis and therapy. However, in Brazilian veterinary medicine, these markers are generally still restricted to researches. This review aims to approach the major cardiac markers, which further may become essential indexes in heart assessment. [ABSTRACT FROM AUTHOR]

An abstract of the article "Evaluation of cardiac dysfunction in an animal model of LPS-induced endotoxic shock," by A. Baumgartner and colleagues is presented.