Post-resuscitation shock was defined as the need for vasoconstric

Post-resuscitation shock was defined as the need for vasoconstrictive drug (epinephrine or norepinephrine) infusion lasting more than 6 hours despite adequate fluid loading. Patient management selleck Perifosine was strictly standardized [2]. When employed, hypothermia was started immediately at ICU admission using external cooling by forced cold air cooling during the first 24 hours in order to obtain a target temperature between 32��C and 34��C. Sedation using adjusted doses of midazolam and morphine or fentanyl, and neuromuscular blocking agent infusion during therapeutic hypothermia, were applied. In the absence of shock or complications, sedation was interrupted at the end of the hypothermia period. Normothermia between 37��C and 37.5��C was then achieved using passive rewarming at the targeted rate of 0.

3��C/hour and maintained during the next 24 hours. Patients with neither admission nor day 1 serum sample were excluded. Part of the cohort was previously studied to investigate PCT levels for the diagnosis of early onset pneumonia after CA; however, patients who died within the first 24 hours, with an infection prior to CA, or with an extra-pulmonary infection developing within 5 days following admission had been excluded [4]. The study was approved by our local Cochin University Hospital institutional review board. Written consent was waived for this study since TRX dosages did not require specific or additional blood drawing. Informed assessment was obtained from all patients or next of kin.

Blood samplingAll TRX measurements were performed in April 2010 by the same investigator (DB) by using blood samples collected at admission, day 1 (D1), day 2 (D2) and day 3 (D3). These samples were initially centrifuged and stored at -80��C within 4 hours, as approved by our local institutional review board, as part of a serum collection. Measurements of TRX were performed in duplicate samples with a commercially available sensitive enzyme-linked immunosorbent assay (Redox Biosciences, Kyoto, Japan). Patients exhibiting hemolysis were excluded due to the high intracellular concentration of TRX, which will bias assessment [7]. Plasma levels of TRX were also determined in 30 healthy volunteers in stable condition at rest (checked for the absence of chronic or acute illness by questionnaire and medical examination). Analyses of CRP were performed with a fully automated immunoturbidimetric Entinostat assay (CRPLX, Modular PP?, Roche Diagnostics, Mannheim, Germany). PCT concentrations were quantified with an immunofluorimetric assay (PCT sensitive, Kryptor?, Brahms, Berlin, Germany).

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