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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 21 (1995), S. 636-640 
    ISSN: 1432-1238
    Keywords: Cardiopulmonary arrest ; Cardiopulmonary resuscitation ; Ischemia ; Neutrophil elastase ; Prognosis ; Urinastatin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective To determine the changes in neutrophil elastase levels in patients with cardiac arrest occurring outside the hospital and to evaluate the effects of urinastatin on these changes and on the clinical outoomes of the patients. Design Prospective study.Setting: The Emergency Department and a general ICU in the tertiary care city hospital. Patients Of the 40 patients who had an out-of-hospital cardiac arrest, 38 of the cases were randomized into 2 groups, with w cases being excluded because of contradiction to protocol. The control and urinastatin groups consisted of 20 and 18 patients, respectively. Interventions Control patients were treated by standard cardiopulmonary resuscitation (CPR) procedures. Patients in the urinastatin group were administered a 100000 U dose of urinastatin immediately after arrival at the Emergency Department and three 100000 U doses at 8h intervals, within the first 24h after resuscitation. Measurements and main results At the time of arrival at the emergency room (before administration of urinastatin), and at 30 min, 60 min, and 24h after, the plasma levels of neutrophil elastase and blood gas levels were determined. Concerning the baseline characteristics of patients, causes of cardiac arrest, time duration of pre-hospital care and treatments given during CPR, there was no difference detected between the control and urinastatin groups. In addition, the pH and PaO2 values showed no differences. Neutrophil elastase values had already increased by the time of arrival and continued to do so until 60 min; at 24h after admission, markedly higher values were obtained. These values were significantly higher in the non-resuscitated cases than in the resuscitated ones. Administration of urinastatin significantly suppressed this increase at 24h, but did not improve the clinical outcomes, including resuscitation rate and survival rate. Conclusions Accompanying cardiopulmonary arrest and resuscitation, neutrophils are activated and elastase is released. Elevated elastase level is associated with poorer prognosis. Urinastatin can suppress the release of elastase, when utilized at the dose described in this study, did not improve the clinical outcomes of patients who had suffered an out-of-hospital cardiac arrest.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1238
    Keywords: Key words Human ; Cardiac arrest ; Cardiopulmonary resuscitation ; Ionized calcium ; Lactate
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To determine the relationship between ionized calcium concentrations and blood lactate levels during cardiac arrest and cardiopulmonary resuscitation (CPR). Design: A prospective cohort study. Setting: Emergency department (ED) and general intensive care unit in a city hospital (tertiary care center). Patients and participants: 32 patients with out-of-hospital cardiac arrest; 14 of the patients had a return of spontaneous circulation (ROSC) and 18 of the patients died. Interventions: Basic and advanced life support. Measurements and results: Concentrations of ionized and total calcium, bicarbonate, lactate, and pyruvate and pH were simultaneously determined immediately upon arrival at the ED, and at 30 and 60 min. Upon arrival at the ED, all patients had ionized hypocalcemia (1.09 ± 0.02 mmol/l). Ionized and total calcium concentrations progressively decreased during and after CPR, but pH and bicarbonate concentrations did not show any significant changes. In patients who had ROSC, a significant, but perhaps not clinically relevant, relationship was observed between the ionized calcium concentrations and pH (r 2 = 0.152, p = 0.0117). In the patients who died, there were significant correlations between ionized calcium and pH (r 2 = 0.382, p = 0.0001) and bicarbonate concentrations (r 2 = 0.298, p = 0.0006). No definite correlations were demonstrated when comparing ionized calcium concentrations with lactate and pyruvate concentrations. Conclusions: Ionized hypocalcemia during out-of-hospital cardiac arrest and CPR is not due to binding by both lactate and pyruvate, but may be partly due to complexing by bicarbonate, with some modifications due to variations in pH.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-1238
    Keywords: Key words Cardiac arrest ; Cardiopulmonary resuscitation ; Platelet aggregation ; Prostaglandin I2 ; Thromboxane A2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: Hypoxia and ischemia cause endothelial cell damage with consequent platelet activation. The hypothesis that human cardiac arrest accelerates platelet activation and the formation of prostanoids was tested. Design: Prospective, observational cohort study. Setting: Emergency Department and general Intensive Care Unit in a city hospital. Interventions: Basic and advanced life support. Patients and participants: Forty-seven out-of-hospital cardiac arrest patients. The patients were classified into two groups, those who were resuscitated (n=18) and those who died (n=29). Measurements and results: Serial levels of platelet aggregation, thromboxane B2 (TXB2), 11-dehydro-TXB2 and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) were measured. The results of measurements and demographic data were compared between the groups. Platelet counts decreased at the end of cardiopulmonary resuscitation (CPR), the decrease of the platelet counts showed statistical significance especially in the patients who died (p〈0.001). Platelet aggregation induced by adenosine diphosphate, epinephrine and collagen decreased to the lower limits of normal during and after CPR. Although high values of TXB2 and 11-dehydro-TXB2 continued throughout the study period in the resuscitated patients, 6-keto-PGF1 alpha decreased to the normal range (22.7±3.6 pg·ml–1, p〈0.05) at 24 h after arrival at the Emergency Department. Conclusions: Platelet activation with the massive formation of thromboxane A2 (TXA2) occurs in patients with out-of-hospital cardiac arrest. Successful resuscitation is not associated with the balanced production of PGI2 against the TXA2 formation.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 25 (1999), S. 588-593 
    ISSN: 1432-1238
    Keywords: Key words Cardiac arrest ; Cardiopulmonary resuscitation ; Selectin ; Neutrophil ; Endothelium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objective: To investigate the relationship between cytokines and the inflammatory responses in patients with out-of-hospital cardiac arrest, we examined the changes of cytokines as well as alterations in the markers of neutrophil activation, platelet and endothelial activation, and endothelial injury. Design: Prospective, cohort study. Setting: General intensive care unit of a tertiary care center. Patients and participants: 26 out-of-hospital cardiac arrest patients were classified into two groups: those who achieved return of spontaneous circulation (ROSC) (n = 10) and those with no ROSC (n = 16). Eight normal healthy volunteers served as control subjects. Measurements and results: Serial levels of soluble L-selectin (sL-selectin), soluble P-selectin (sP-selectin), neutrophil elastase, and soluble thrombomodulin were measured during and after cardiopulmonary resuscitation (CPR). Serial levels of tumor necrosis factor α (TNFα) and interleukin-1β (IL-1β) were also measured. We could not find any elevations in either cytokine during the study period. In both groups, sP-selectin levels were significantly higher than those in control subjects from the time of arrival at the emergency department to 24 h after admission. sL-selectin levels in the two groups were markedly lower compared to those in control subjects at all sampling points. In patients with ROSC, cardiac arrest and CPR led to an increase in the levels of neutrophil elastase and soluble thrombomodulin that peaked 6 h or 24 h after arrival at the emergency department. No statistical differences in the levels of the two selectins, neutrophil elastase, and soluble thrombomodulin between the two groups were found during CPR. Conclusions: Out-of-hospital cardiac arrest and CPR induces platelet, neutrophil, and endothelial activation and is associated with endothelial injury. Inflammatory cytokines may not have an important role in human whole-body ischemia-reperfusion injury.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Intensive care medicine 26 (2000), S. 487-487 
    ISSN: 1432-1238
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-1238
    Keywords: Key words Cardiac arrest ; Cardiopulmonary resuscitation ; Soluble adhesion molecules ; Neutrophil ; Endothelium
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Objectives: To investigate the inflammatory responses in patients with out-of-hospital cardiac arrest, we examined the changes in markers of endothelial activation, neutrophil activation, and endothelial injury.¶Design: Prospective, cohort study.¶Setting: General intensive care unit of a tertiary care center.¶Patients and participants: Forty-four out-of-hospital cardiac arrest patients were classified into two groups, those who achieved return of spontaneous circulation (ROSC) (n = 23) and those without ROSC (n = 21). Eight normal healthy volunteers served as control subjects.¶Measurements and results: Serial levels of soluble intercellular adhesion molecule-1 (sICAM-1), soluble vascular cell adhesion molecule-1 (sVCAM-1), soluble E-selectin (sE-selectin) as markers of endothelial activation, neutrophil elastase as a marker of neutrophil activation, and soluble thrombomodulin as a marker of endothelial injury were measured during and after cardiopulmonary resuscitation (CPR). In patients with ROSC, cardiac arrest and CPR led to increases in the levels of three vascular endothelial adhesion molecules, neutrophil elastase, and soluble thrombomodulin that peaked 6 h or 24 h after arrival at the emergency department. In patients without ROSC, only neutrophil elastase showed moderate elevation during CPR. We could not find significant differences in all measured parameters between the two groups.¶Conclusions: As evidence of inflammatory responses in whole-body ischemia and reperfusion, our study demonstrates neutrophil-endothelium interaction with signs of endothelial injury in patients with out-of-hospital cardiac arrest. These inflammatory changes may have an important role in post-resuscitation syndrome after human cardiac arrest.
    Type of Medium: Electronic Resource
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