Abstract
IntroductionWhole-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.MethodsTen 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.ResultsThe 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.ConclusionsProlonged 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.
Highlights
Whole-body ischemia and reperfusion trigger a systemic inflammatory response
We demonstrated that complement activation and a proinflammatory response occur during rewarming after 24-hour induction of mild hypothermia after cardiac arrest [10]
Population We studied ten comatose patients successfully resuscitated from an out-of-hospital cardiac arrest
Summary
We analyzed the effect of temperature on the inflammatory response in patients treated with prolonged mild hypothermia after cardiac arrest. The post–cardiac arrest phase is characterized by high levels of circulating cytokines and adhesion molecules, the presence of plasma endotoxins, and dysregulated leukocyte production of cytokines and complement activation. The mechanisms underlying this postresuscitation disease involve a whole-body ischemia and reperfusion syndrome that triggers a systemic inflammatory response mimicking the immunologic and coagulation disorders observed in severe sepsis [5]. We demonstrated that complement activation and a proinflammatory response occur during rewarming after 24-hour induction of mild hypothermia after cardiac arrest [10]. We describe the inflammatory response over time in patients treated with therapeutic hypothermia for an extended period of 72 hours after cardiac arrest
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