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dc.contributor.authorBisschops, Laurens L.A.
dc.contributor.authorvan der Hoeven, Johannes G.
dc.contributor.authorMollnes, Tom Eirik
dc.contributor.authorHoedemaekers, Cornelia W.E.
dc.date.accessioned2022-05-19T10:48:03Z
dc.date.available2022-05-19T10:48:03Z
dc.date.issued2014-10-11
dc.description.abstractIntroduction: Whole-body ischemia and reperfusion trigger a systemic inflammatory response. In this study, we analyzed the effect of temperature on the inflammatory response in patients treated with prolonged mild hypothermia after cardiac arrest.<p> <p>Methods: Ten comatose patients with return of spontaneous circulation after pulseless electrical activity/asystole or prolonged ventricular fibrillation were treated with mild therapeutic hypothermia for 72 hours after admission to a tertiary care university hospital. At admission and at 12, 24, 36, 48, 72, 96 and 114 hours, the patients’ temperature was measured and blood samples were taken from the arterial catheter. Proinflammatory interleukin 6 (IL-6) and anti-inflammatory (IL-10) cytokines and chemokines (IL-8 and monocyte chemotactic protein 1), intercellular adhesion molecule 1 and complement activation products (C1r-C1s-C1inhibitor, C4bc, C3bPBb, C3bc and terminal complement complex) were measured. Changes over time were analyzed with the repeated measures test for nonparametric data. Dunn’s multiple comparisons test was used for comparison of individual time points. <p>Results: The median temperature at the start of the study was 34.3°C (33.4°C to 35.2°C) and was maintained between 32°C and 34°C for 72 hours. All patients were passively rewarmed after 72 hours, from (median (IQR)) 33.7°C (33.1°C to 33.9°C) at 72 hours to 38.0°C (37.5°C to 38.1°C) at 114 hours (P <0.001). In general, the cytokines and chemokines remained stable during hypothermia and decreased during rewarming, whereas complement activation was suppressed during the whole hypothermia period and increased modestly during rewarming. <p>Conclusions: Prolonged hypothermia may blunt the inflammatory response after rewarming in patients after cardiac arrest. Complement activation was low during the whole hypothermia period, indicating that complement activation is also highly temperature-sensitive in vivo. Because inflammation is a strong mediator of secondary brain injury, a blunted proinflammatory response after rewarming may be beneficial.en_US
dc.identifier.citationBisschops LL, van der Hoeven JG, Mollnes TE, Hoedemaekers CW. Seventy-two hours of mild hypothermia after cardiac arrest is associated with a lowered inflammatory response during rewarming in a prospective observational study. Critical Care. 2014;18(546)en_US
dc.identifier.cristinIDFRIDAID 1192343
dc.identifier.doi10.1186/s13054-014-0546-5
dc.identifier.issn1364-8535
dc.identifier.issn1466-609X
dc.identifier.urihttps://hdl.handle.net/10037/25225
dc.language.isoengen_US
dc.publisherBMCen_US
dc.relation.journalCritical Care
dc.relation.urihttp://ccforum.com/content/18/5/546
dc.rights.accessRightsopenAccessen_US
dc.rights.holderCopyright 2014 The Author(s)en_US
dc.titleSeventy-two hours of mild hypothermia after cardiac arrest is associated with a lowered inflammatory response during rewarming in a prospective observational studyen_US
dc.type.versionpublishedVersionen_US
dc.typeJournal articleen_US
dc.typeTidsskriftartikkelen_US
dc.typePeer revieweden_US


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