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  • Scholz, Jens  (38)
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  • 1
    Language: English
    In: European Journal of Pharmacology, 2010, Vol.645(1), pp.39-46
    Description: Using animal models, volatile anesthetics have been recognized for their neuroprotective effects. Nevertheless, there is still disagreement about the optimal duration and timing of conditioning with the volatile anesthetic sevoflurane in the human system. In the study presented, we employed a human neuronal cell culture model to investigate the effects of hypoxia and to evaluate potential cytoprotective properties of different sevoflurane conditioning strategies. Sevoflurane was applied to human IMR-32 cells in which hypoxic conditions were induced for 2 h using our recently described two-enzyme model (Zitta et al., Eur. J. Pharmacol., 2010). Cellular effects of hypoxia and sevoflurane conditioning were evaluated by lactate dehydrogenase (LDH) measurements, brightfield microscopy, ELISAs, cytometric bead arrays, Westernblotting and RT-PCR. Hypoxia increased the release of LDH into the culture medium after 24 h (normoxia: 0.15 ± 0.02 a.u; hypoxia: 0.69 ± 0.08 a.u, P 〈 0.001) and expression of hypoxia associated genes HIF-1alpha, VEGF, catalase. Cytoprotective effects were observed in cultures that received sevoflurane for 30 min before hypoxia (preconditioning: 0.41 ± 0.07 a.u., P 〈 0.01) and for 30 min during the hypoxic period (intraconditioning: 0.20 ± 0.01 a.u., P 〈 0.001). Application of sevoflurane after the hypoxic insult did not lead to cytoprotection (postconditioning: 0.73 ± 0.12 a.u., P 〉 0.05). Conditioning with sevoflurane for a total of 3 h before, during and after hypoxia, however, resulted in an enhanced release of LDH (periconditioning: 0.97 ± 0.10 a.u., P 〈 0.01) and additional cell damage. Hypoxia and sevoflurane intraconditioning were associated with changes in erk1/2 phosphorylation (T202/Y204) and HIF-1alpha protein levels, whereas phosphorylation of akt (S473) was not significantly altered. Our results suggest short pre- and intraconditioning with sevoflurane as most potent strategies to reduce hypoxia induced neuronal cell damage.
    Keywords: Hypoxia ; Pharmacological Conditioning ; Volatile Anesthetic ; Sevoflurane ; Cell Culture ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0014-2999
    E-ISSN: 1879-0712
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  • 2
    Language: English
    In: Journal of translational medicine, 27 January 2015, Vol.13, pp.34
    Description: Transient episodes of ischemia in a remote organ (remote ischemic preconditioning, RIPC) can attenuate myocardial ischemia/reperfusion injury but the underlying mechanisms of RIPC in the target organ are still poorly understood. Recent animal studies suggested that the small redox protein thioredoxin may be a potential candidate for preconditioning-induced organprotection. Here we employed a human proteome profiler array to investigate the RIPC regulated expression of cell stress proteins and particularly of thioredoxin in heart tissue of cardiosurgical patients with cardiopulmonary bypass (CPB). RIPC was induced by four 5 minute cycles of transient upper limb ischemia/reperfusion using a blood pressure cuff. Right atrial tissue was obtained from patients receiving RIPC (N = 19) and control patients (N = 19) before and after CPB. Cell stress proteome profiler arrays as well as Westernblotting and ELISA experiments for thioredoxin (Thio-1) were performed employing the respective tissue samples. Protein arrays revealed an up-regulation of 26.9% (7/26; CA IX, Cyt C, HSP-60, HSP-70, pJNK, SOD2, Thio-1) of cell stress associated proteins in RIPC tissue obtained before CPB, while 3.8% (1/26; SIRT2) of the proteins were down-regulated. Array results for thioredoxin were verified by semi-quantitative Westernblotting studies which showed a significant up-regulation of thioredoxin protein levels in cardiac tissue samples of RIPC patients taken before CPB (RIPC: 5.36 ± 0.85 a.u.; control: 3.23 ± 0.39 a.u.; P 〈 0.05). Quantification of thioredoxin levels in tissue of RIPC and control patients by ELISA experiments further confirmed the Westernblotting results (RIPC: 0.30 ± 0.02 ng/mg protein; control: 0.24 ± 0.02 ng/mg protein; P 〈 0.05). We provide evidence for thioredoxin as a RIPC-induced factor in heart tissue of cardiosurgical patients and identified several cell stress associated proteins that are regulated by RIPC and may play a role in RIPC-mediated cardioprotection.
    Keywords: Cardiovascular Surgical Procedures ; Ischemic Preconditioning ; Proteomics ; Stress, Physiological ; Cardiotonic Agents -- Metabolism ; Myocardium -- Metabolism ; Thioredoxins -- Metabolism
    E-ISSN: 1479-5876
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  • 3
    Language: English
    In: European Journal of Pharmacology, 2010, Vol.628(1), pp.11-18
    Description: Mild hypothermia and pharmacological postconditioning are widespread therapeutical treatment options that positively influence the clinical outcome after tissue hypoxia. In the study presented, a two-enzyme based oxygen deficiency model in combination with cultured HT-1080 fibrosarcoma cells was employed to mimic the situation of hypoxia and to evaluate the influence of mild hypothermia and postconditioning with catalase on hypoxia-mediated cell damage. Using the oxygen deficiency model, partial pressure of oxygen was rapidly reduced to levels below 5 mmHg in the culture media and cells responded with an increased expression of hypoxia inducible factor-1 on protein level. Hypoxia resulted in significant cell rounding and retraction of cytoplasmic cell extensions. Evaluation of cytotoxicity revealed a 3.5-fold increase in lactate dehydrogenase levels which was accompanied by 40-fold elevated levels of hydrogen peroxide. The hypoxia-induced increase of lactate dehydrogenase was 2.5-fold reduced in the hypothermia group, although morphological correlates of cytotoxicity were still visible. Hypothermia did not significantly influence hydrogen peroxide concentrations in the culture media. Pharmacological postconditioning with catalase however dose-dependently decreased hypoxia-induced lactate dehydrogenase release. This cytoprotective effect was accompanied by a dose-dependent, up to 50-fold reduction of hydrogen peroxide concentrations and retention of normal cell morphology. We suggest that the described oxygen deficiency model is a convenient and simple culture system for the investigation of cellular and subcellular events associated with oxygen deficiency. Moreover, our results imply that catalase postconditioning may be a promising approach to attenuate hypoxia-induced and hydrogen peroxide-mediated cell and tissue damage.
    Keywords: Hypoxia ; Postconditioning ; Catalase ; Mild Hypothermia ; Hydrogen Peroxide ; Reactive Oxygen Species ; Pharmacy, Therapeutics, & Pharmacology
    ISSN: 0014-2999
    E-ISSN: 1879-0712
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  • 4
    Language: English
    In: Resuscitation, January 2012, Vol.83(1), pp.113-118
    Description: Successful resuscitation after cardiac arrest is typically associated with cerebral and myocardial ischemia/reperfusion (I/R)-injury. Recently, we have demonstrated effects of therapeutic hypothermia (HT) and postconditioning with the volatile anesthetic sevoflurane (SEV) on I/R-mediated mechanisms in the heart and brain [Meybohm et al., PLoS One, 2009; Meybohm et al., Crit Care, 2010]. As the intestine is also highly susceptible to I/R-injury, we investigated the influence of HT and SEV on intestinal I/R-mediated events induced by cardiac arrest and successful resuscitation. Effects of I/R, HT (12 h, 33 °C) and a combination of HT with SEV (12 h, 2.0 vol%) were evaluated in a pig model of cardiac arrest and successful cardiopulmonary resuscitation. Western blotting, ELISA, caspase-3/7 assays, myeloperoxidase (MPO) quantifications and gelatine zymography were performed using intestinal tissue derived 24 h after return of spontaneous circulation. Compared to the normothermia control, HT and HT + SEV resulted in a significant increase in intestinal HIF-1α protein expression ( 〈 0.05). Tissue concentrations of IL-1β were significantly reduced in the HT and HT + SEV group ( 〈 0.05), whereas a reduction of IL-10 levels was only detected in the intestine of animals treated with HT + SEV ( 〈 0.05). A statistically significant increase of intestinal MPO activity was found in the HT + SEV group ( 〈 0.01). Activities of caspase-3 and 7 or matrixmetalloproteinase-2 were not changed in any of the groups investigated, the activity of matrixmetalloproteinase-9 was, however, significantly increased in the HT + SEV group ( 〈 0.05). HT and postconditioning with SEV influence the expression and activity of several small intestinal proteins that are possibly involved in intestinal I/R-mediated events following successful cardiopulmonary resuscitation.
    Keywords: Therapeutic Hypothermia ; Anesthetic Postconditioning ; Intestine ; Ischemia/Reperfusion ; Medicine
    ISSN: 0300-9572
    E-ISSN: 1873-1570
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  • 5
    In: Circulation, 2010, Vol.122(21_MeetingAbstracts Suppl 1)
    Description: Background: Both myocardial and neurological dysfunctions are critical issues after successful cardiopulmonary resuscitation (CPR). Volatile anesthetics have been suggested to be both cardio- and neuroprotective in ischemia/reperfusion injury.Methods: Twenty anesthetized (4 mg/kg/h propofol) pigs were subjected to electrically-induced cardiac arrest. After 8 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started according to the current AHA guidelines. After successful return of spontaneous circulation (ROSC; n=16), animals were randomized either to i) continuing 4 mg/kg/h propofol anesthesia (Control) or to ii) the volatile anesthetic sevoflurane (2.0 Vol% SEVO). Animals were weaned from the ventilator 4h after ROSC. 24h after ROSC, first neurological performance was evaluated using a neurological deficit score (CCM 1994; 22: 282–90). Then, pigs were again anesthetized with propofol in order to obtain left ventricular ejection fraction (LVEF) by transesophageal echocardiography and to take cardiac and cerebral cortex tissue samples. Serum troponin T levels were determined. The effects on cardiac and cerebral tissue interleukin (IL)-1β protein expression were studied using ELISA technique.Results: Animals treated with SEVO showed increased LVEF, lower troponin T peak levels (Fig. 1a,b; p〈0.05) and reduced cardiac IL-1β protein expression levels (0.12±0.01 vs. 0.15±0.02 pg/ total protein in μg; p〈0.05) compared to the Control group. Neurological deficit scores (Fig. 1c) and cerebral IL-1β protein expression levels did not differ between groups.Conclusions: After cardiopulmonary resuscitation, the application of the volatile anesthetic sevoflurane showed postconditioning effects by reducing myocardial damage and dysfunction possible via a reduced rate of pro-inflammatory cytokine expression, but did not improve neurological deficits.(Figure is included in full-text article.)
    ISSN: 0009-7322
    Source: Copyright © 2013 Lippincott Williams & Wilkins. All rights reserved.〈img src=http://exlibris-pub.s3.amazonaws.com/LWW%20logo.png style="vertical-align:middle;margin-left:7px"〉
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  • 6
    Language: English
    In: PLoS ONE, May 31, 2013, Vol.8(5), p.e64743
    Description: Background Remote ischemic preconditioning (RIPC) has been shown to enhance the tolerance of remote organs to cope with a subsequent ischemic event. We hypothesized that RIPC reduces postoperative neurocognitive dysfunction (POCD) in patients undergoing complex cardiac surgery. Methods We conducted a prospective, randomized, double-blind, controlled trial including 180 adult patients undergoing elective cardiac surgery with cardiopulmonary bypass. Patients were randomized either to RIPC or to control group. Primary endpoint was postoperative neurocognitive dysfunction 5-7 days after surgery assessed by a comprehensive test battery. Cognitive change was assumed if the preoperative to postoperative difference in 2 or more tasks assessing different cognitive domains exceeded more than one SD (1 SD criterion) or if the combined Z score was 1.96 or greater (Z score criterion). Results According to 1 SD criterion, 52% of control and 46% of RIPC patients had cognitive deterioration 5-7 days after surgery (p = 0.753). The summarized Z score showed a trend to more cognitive decline in the control group (2.16#177;5.30) compared to the RIPC group (1.14#177;4.02; p = 0.228). Three months after surgery, incidence and severity of neurocognitive dysfunction did not differ between control and RIPC. RIPC tended to decrease postoperative troponin T release at both 12 hours [0.60 (0.19-1.94) [micro]g/L vs. 0.48 (0.07-1.84) [micro]g/L] and 24 hours after surgery [0.36 (0.14-1.89) [micro]g/L vs. 0.26 (0.07-0.90) [micro]g/L]. Conclusions We failed to demonstrate efficacy of a RIPC protocol with respect to incidence and severity of POCD and secondary outcome variables in patients undergoing a wide range of cardiac surgery. Therefore, definitive large-scale multicenter trials are needed. Trial Registration ClinicalTrials.gov NCT00877305
    Keywords: Ischemia -- Research ; Troponin ; Surgery ; Clinical Trials ; Batteries ; Cardiac Patients ; Coronary Artery Bypass
    ISSN: 1932-6203
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  • 7
    Language: English
    In: Critical Care, Oct 19, 2011, Vol.15, p.R241
    Description: Introduction In this study, we sought to examine whether pharmacological postconditioning with sevoflurane (SEVO) is neuro- and cardioprotective in a pig model of cardiopulmonary resuscitation. Methods Twenty-two pigs were subjected to cardiac arrest. After 8 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started. After successful return of spontaneous circulation (N = 16), animals were randomized to either (1) propofol (CONTROL) anesthesia or (2) SEVO anesthesia for 4 hours. Neurological function was assessed 24 hours after return of spontaneous circulation. The effects on myocardial and cerebral damage, especially on inflammation, apoptosis and tissue remodeling, were studied using cellular and molecular approaches. Results Animals treated with SEVO had lower peak troponin T levels (median [IQR]) (CONTROL vs SEVO = 0.31 pg/mL [0.2 to 0.65] vs 0.14 pg/mL [0.09 to 0.25]; P [less than] 0.05) and improved left ventricular systolic and diastolic function compared to the CONTROL group (P [less than] 0.05). SEVO was associated with a reduction in myocardial IL-1[beta] protein concentrations (0.16 pg/[mu]g total protein [0.14 to 0.17] vs 0.12 pg/[mu]g total protein [0.11 to 0.14]; P [less than] 0.01), a reduction in apoptosis (increased procaspase-3 protein levels (0.94 arbitrary units [0.86 to 1.04] vs 1.18 arbitrary units [1.03 to 1.28]; P [less than] 0.05), increased hypoxia-inducible factor (HIF)-1[alpha] protein expression (P [less than] 0.05) and increased activity of matrix metalloproteinase 9 (P [less than] 0.05). SEVO did not, however, affect neurological deficit score or cerebral cellular and molecular pathways. Conclusions SEVO reduced myocardial damage and dysfunction after cardiopulmonary resuscitation in the early postresuscitation period. The reduction was associated with a reduced rate of myocardial proinflammatory cytokine expression, apoptosis, increased HIF-1[alpha] expression and increased activity of matrix metalloproteinase 9. Early administration of SEVO may not, however, improve neurological recovery.
    Keywords: Sevoflurane -- Dosage And Administration ; Sevoflurane -- Research ; Cardiovascular Conditioning -- Research ; Cardiopulmonary Resuscitation -- Complications And Side Effects ; Cardiopulmonary Resuscitation -- Patient Outcomes ; Cardiopulmonary Resuscitation -- Research ; Myocardial Diseases -- Prevention ; Myocardial Diseases -- Research ; Nervous System Diseases -- Prevention ; Nervous System Diseases -- Research
    ISSN: 1364-8535
    Source: Cengage Learning, Inc.
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  • 8
    Language: English
    In: Critical Care, Oct 19, 2011, Vol.15, p.R241
    Description: Introduction In this study, we sought to examine whether pharmacological postconditioning with sevoflurane (SEVO) is neuro- and cardioprotective in a pig model of cardiopulmonary resuscitation. Methods Twenty-two pigs were subjected to cardiac arrest. After 8 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started. After successful return of spontaneous circulation (N = 16), animals were randomized to either (1) propofol (CONTROL) anesthesia or (2) SEVO anesthesia for 4 hours. Neurological function was assessed 24 hours after return of spontaneous circulation. The effects on myocardial and cerebral damage, especially on inflammation, apoptosis and tissue remodeling, were studied using cellular and molecular approaches. Results Animals treated with SEVO had lower peak troponin T levels (median [IQR]) (CONTROL vs SEVO = 0.31 pg/mL [0.2 to 0.65] vs 0.14 pg/mL [0.09 to 0.25]; P [less than] 0.05) and improved left ventricular systolic and diastolic function compared to the CONTROL group (P [less than] 0.05). SEVO was associated with a reduction in myocardial IL-1[beta] protein concentrations (0.16 pg/[mu]g total protein [0.14 to 0.17] vs 0.12 pg/[mu]g total protein [0.11 to 0.14]; P [less than] 0.01), a reduction in apoptosis (increased procaspase-3 protein levels (0.94 arbitrary units [0.86 to 1.04] vs 1.18 arbitrary units [1.03 to 1.28]; P [less than] 0.05), increased hypoxia-inducible factor (HIF)-1[alpha] protein expression (P [less than] 0.05) and increased activity of matrix metalloproteinase 9 (P [less than] 0.05). SEVO did not, however, affect neurological deficit score or cerebral cellular and molecular pathways. Conclusions SEVO reduced myocardial damage and dysfunction after cardiopulmonary resuscitation in the early postresuscitation period. The reduction was associated with a reduced rate of myocardial proinflammatory cytokine expression, apoptosis, increased HIF-1[alpha] expression and increased activity of matrix metalloproteinase 9. Early administration of SEVO may not, however, improve neurological recovery.
    Keywords: Cardiopulmonary Resuscitation -- Analysis ; Apoptosis -- Analysis ; Anesthesia -- Analysis ; Inflammation -- Analysis ; Troponin -- Analysis
    ISSN: 1364-8535
    Source: Cengage Learning, Inc.
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  • 9
    Language: English
    In: Critical Care, Nov 24, 2011, Vol.15, p.R282
    Description: Introduction Sudden cardiac arrest is one of the most frequent causes of death in the world. In highly qualified emergency medical service (EMS) systems, including well-trained emergency physicians, spontaneous circulation may be restored in up to 53% of patients at least until admission to hospital. Compared with these highly qualified EMS systems, markedly lower success rates are observed in other systems. These data clearly show that there are considerable differences between EMS systems concerning treatment success following cardiac arrest and resuscitation, although in all systems international guidelines for resuscitation are used. In this study, we investigated the impact of response time reliability (RTR) on cardiopulmonary resuscitation (CPR) incidence and resuscitation success by using the return of spontaneous circulation (ROSC) after cardiac arrest (RACA) scores and data from seven German EMS systems participating in the German Resuscitation Registry. Methods Anonymised patient data after out-of-hospital cardiac arrest gathered from seven EMS systems in Germany from 2006 to 2009 were analysed with regard to socioeconomic factors (population, area and EMS unit-hours), process quality (RTR, CPR incidence, special CPR measures and prehospital cooling), patient factors (age, gender, cause of cardiac arrest and bystander CPR). End points were defined as ROSC, admission to hospital, 24-hour survival and hospital discharge rate. [chi].sup.2 .sup.tests, odds ratios and the Bonferroni correction were used for statistical analyses. Results Our present study comprised 2,330 prehospital CPR patients at seven centres. The incidence of sudden cardiac arrest ranged from 36.0 to 65.1/100,000 inhabitants/year. We identified two EMS systems (RTR [less than] 70%) that reached patients within 8 minutes of the call to the dispatch centre 62.0% and 65.6% of the time, respectively. The other five EMS systems (RTR 〉 70%) reached patients within 8 minutes of the call to the dispatch centre 70.4% up to 95.5% of the time. EMS systems arriving relatively later at the patients side (RTR [less than] 70%) initiate CPR less frequently and admit fewer patients alive to hospital (calculated per 100,000 inhabitants/year) (CPR incidence (1/100,000 inhabitants/year) RTR 〉 70% = 57.2 vs RTR [less than] 70% = 36.1, OR = 1.586 (99% CI = 1.383 to 1.819); P [less than] 0.01) (admitted to hospital with ROSC (1/100,000 inhabitants/year) RTR 〉 70% = 24.4 vs RTR [less than] 70% = 15.6, OR = 1.57 (99% CI = 1.274 to 1.935); P [less than] 0.01). Using ROSC rate and the multivariate RACA score to predict outcomes, we found that the two groups did not differ, but ROSC rates were higher than predicted in both groups (ROSC RTR 〉 70% = 46.6% vs RTR [less than] 70% = 47.3%, OR = 0.971 (95% CI = 0.787 to 1.196); P = n.s.) (ROSC RACA RTR 〉 70% = 42.4% vs RTR [less than] 70% = 39.5%, OR = 1.127 (95% CI = 0.911 to 1.395); P = n.s.) Conclusion This study demonstrates that, on the level of EMS systems, faster ones more often initiate CPR and increase the number of patients admitted to hospital alive. Furthermore, we show that, with very different approaches, all centres that adhere to and are intensely trained according to the 2005 European Resuscitation Council guidelines are superior and, on the basis of international comparisons, achieve excellent success rates following CPR.
    Keywords: Emergency Medical Services -- Research ; Emergency Medical Services -- Analysis ; Cardiopulmonary Resuscitation -- Research ; Cardiopulmonary Resuscitation -- Analysis ; Cardiology -- Research ; Cardiology -- Analysis
    ISSN: 1364-8535
    Source: Cengage Learning, Inc.
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  • 10
    Language: English
    In: Critical Care, Nov 24, 2011, Vol.15, p.R282
    Description: Introduction Sudden cardiac arrest is one of the most frequent causes of death in the world. In highly qualified emergency medical service (EMS) systems, including well-trained emergency physicians, spontaneous circulation may be restored in up to 53% of patients at least until admission to hospital. Compared with these highly qualified EMS systems, markedly lower success rates are observed in other systems. These data clearly show that there are considerable differences between EMS systems concerning treatment success following cardiac arrest and resuscitation, although in all systems international guidelines for resuscitation are used. In this study, we investigated the impact of response time reliability (RTR) on cardiopulmonary resuscitation (CPR) incidence and resuscitation success by using the return of spontaneous circulation (ROSC) after cardiac arrest (RACA) scores and data from seven German EMS systems participating in the German Resuscitation Registry. Methods Anonymised patient data after out-of-hospital cardiac arrest gathered from seven EMS systems in Germany from 2006 to 2009 were analysed with regard to socioeconomic factors (population, area and EMS unit-hours), process quality (RTR, CPR incidence, special CPR measures and prehospital cooling), patient factors (age, gender, cause of cardiac arrest and bystander CPR). End points were defined as ROSC, admission to hospital, 24-hour survival and hospital discharge rate. [chi].sup.2 .sup.tests, odds ratios and the Bonferroni correction were used for statistical analyses. Results Our present study comprised 2,330 prehospital CPR patients at seven centres. The incidence of sudden cardiac arrest ranged from 36.0 to 65.1/100,000 inhabitants/year. We identified two EMS systems (RTR [less than] 70%) that reached patients within 8 minutes of the call to the dispatch centre 62.0% and 65.6% of the time, respectively. The other five EMS systems (RTR 〉 70%) reached patients within 8 minutes of the call to the dispatch centre 70.4% up to 95.5% of the time. EMS systems arriving relatively later at the patients side (RTR [less than] 70%) initiate CPR less frequently and admit fewer patients alive to hospital (calculated per 100,000 inhabitants/year) (CPR incidence (1/100,000 inhabitants/year) RTR 〉 70% = 57.2 vs RTR [less than] 70% = 36.1, OR = 1.586 (99% CI = 1.383 to 1.819); P [less than] 0.01) (admitted to hospital with ROSC (1/100,000 inhabitants/year) RTR 〉 70% = 24.4 vs RTR [less than] 70% = 15.6, OR = 1.57 (99% CI = 1.274 to 1.935); P [less than] 0.01). Using ROSC rate and the multivariate RACA score to predict outcomes, we found that the two groups did not differ, but ROSC rates were higher than predicted in both groups (ROSC RTR 〉 70% = 46.6% vs RTR [less than] 70% = 47.3%, OR = 0.971 (95% CI = 0.787 to 1.196); P = n.s.) (ROSC RACA RTR 〉 70% = 42.4% vs RTR [less than] 70% = 39.5%, OR = 1.127 (95% CI = 0.911 to 1.395); P = n.s.) Conclusion This study demonstrates that, on the level of EMS systems, faster ones more often initiate CPR and increase the number of patients admitted to hospital alive. Furthermore, we show that, with very different approaches, all centres that adhere to and are intensely trained according to the 2005 European Resuscitation Council guidelines are superior and, on the basis of international comparisons, achieve excellent success rates following CPR.
    Keywords: Emergency Medical Services -- Research ; Emergency Medical Services -- Analysis ; Cardiopulmonary Resuscitation -- Research ; Cardiopulmonary Resuscitation -- Analysis ; Cardiology -- Research ; Cardiology -- Analysis
    ISSN: 1364-8535
    Source: Cengage Learning, Inc.
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