| Rewarming after hypothermia after cardiac arrest shifts the inflammatory balance. | |
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MedLine Citation:
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PMID: 22020246 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVES: The aim of this study was to simultaneously analyze the key components of the cerebral and systemic inflammatory response over time in cardiac arrest patients during mild therapeutic hypothermia and rewarming. DESIGN AND SETTING: Clinical observational study in a tertiary care university hospital. PATIENTS: Ten comatose patients after out-of-hospital cardiac arrest. INTERVENTIONS: All patients were cooled to 32-34°C for 24 hrs. After 24 hrs patients were passively rewarmed to normothermia. MEASUREMENTS AND MAIN RESULTS: On admission and at 3, 6, 12, 24, and 48 hrs blood samples were taken from the arterial and jugular bulb catheter. Proinflammatory and anti-inflammatory cytokines and chemokines (interleukin-1ra, interleukin-1β, interleukin-6, interleukin-8, interleukin-10, interleukin-18, monocyte chemotactic protein-1, high-mobility group box-1 and tumor necrosis factor-α), complement activation products (C4d, Bb, C3a, and terminal complement complex), and the adhesion molecule soluble intercellular adhesion molecule were measured. Mean temperatures at the start of the study and at 12 and 24 hrs were 33.7 ± 0.9°C, 32.7 ± 0.92°C, and 34.5 ± 1.5°C, respectively. Passive rewarming resulted in a temperature of 37.8 ± 0.5°C at 48 hrs. The proinflammatory cytokine interleukin-6 increased from 12 to 24 hrs and returned to baseline levels after 48 hrs. In contrast, the chemokines interleukin-8 and monocyte chemotactic protein-1 stayed relatively high from the start and during the hypothermia period, decreasing to baseline levels after 48 hrs. The anti-inflammatory cytokines interleukin-10 and interleukin-1ra did not significantly change during mild therapeutic hypothermia and rewarming, although low values of interleukin-10 were observed after rewarming. A significant increase after rewarming was demonstrated on high-mobility group box-1 concentrations in the jugular bulb, whereas soluble intercellular adhesion molecule increased significantly during hypothermia and remained at this level after rewarming. Complement activation was increased on admission and decreased after induction of hypothermia, followed by a secondary increase during rewarming. No significant differences between any of the biomarkers were found between samples from the arterial and jugular bulb catheter. CONCLUSIONS: Complement activation occurs during rewarming from mild therapeutic hypothermia after cardiac arrest. Interleukin-6 increased already from 12 to 24 hrs, concomitantly with a significant increase in the temperature seen during this period of mild therapeutic hypothermia. The optimal rate of rewarming is unknown. Additional clinical studies are needed to determine the optimal rewarming rate and strategy. |
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Authors:
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Laurens L A Bisschops; Cornelia W E Hoedemaekers; Tom E Mollnes; Johannes G van der Hoeven |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Critical care medicine Volume: 40 ISSN: 1530-0293 ISO Abbreviation: Crit. Care Med. Publication Date: 2012 Apr |
Date Detail:
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Created Date: 2012-03-19 Completed Date: 2012-05-07 Revised Date: 2012-12-14 |
Medline Journal Info:
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Nlm Unique ID: 0355501 Medline TA: Crit Care Med Country: United States |
Other Details:
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Languages: eng Pagination: 1136-42 Citation Subset: AIM; IM |
Affiliation:
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Department of Intensive Care, Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands. L.Bisschops@ic.umcn.nl |
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| MeSH Terms | |
Descriptor/Qualifier:
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Aged Cell Adhesion Molecules / blood Chemokines / blood Complement Activation Cytokines / blood Female Humans Hypothermia, Induced* Inflammation / immunology, prevention & control* Interleukin-6 / blood Male Out-of-Hospital Cardiac Arrest / immunology, therapy* Prospective Studies Rewarming* Time Factors |
| Chemical | |
Reg. No./Substance:
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0/Cell Adhesion Molecules; 0/Chemokines; 0/Cytokines; 0/Interleukin-6 |
| Comments/Corrections | |
Comment In:
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Crit Care Med. 2012 Apr;40(4):1349-51
[PMID:
22425836
]
Crit Care Med. 2012 Nov;40(11):3105; author reply 3105-6 [PMID: 23080452 ] |
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