This may promote, at least in part, neuroprotection. (iii) The volatile anesthetic sevoflurane, when administered during reperfusion after successful CPR, did not confer statistically significant additional anti-inflammatory effects in the above setting.Key messages? Global cerebral ischemia following selleck Erlotinib cardiac arrest results in up-regulation of local pro-inflammatory cytokines expression.? Mild hypothermia after cardiac arrest attenuates cerebral inflammatory response.? Sevoflurane does not confer additional anti-inflammatory effects.? Further studies on the relationship between cerebral inflammatory response and post-resuscitation cerebral dysfunction are warranted.

AbbreviationsBL: baseline; CPR: cardiopulmonary resuscitation; ELISA: enzyme-linked immunosorbent assay; HT: hypothermia; ICAM-1: intercellular adhesion molecule-1; IL: interleukin; LAD: left anterior descending (coronary artery); NT: normothermia; ROSC: return of spontaneous circulation; RT-PCR: reverse transcriptase polymerase chain reaction; SEV: sevoflurane; TIVA: total intravenous anesthesia; TNF��: tumor necrosis factor ��; VF: ventricular fibrillation.Competing interestsThe authors declare that they have no competing interests.Authors’ contributionsPM, KDZ and BB conceived and designed the experiments. PM, MG, KDZ and MA performed the experiments. MG, MA, RL, NF, JH and KZ analyzed the data. PM, KDZ, MA and BB wrote the paper. All authors read and approved the final manuscript.Supplementary MaterialAdditional file 1:Extended Method section – Quantitative real-time RT-PCR.

Detailed description of quantitative real-time RT-PCR, primer sequences and TaqMan probes.Click here for file(80K, doc)NotesSee related commentary by Zhang, http://ccforum.com/content/14/2/137AcknowledgementsThis work has been supported by the German Interdisciplinary Association of Critical Care Medicine (PM) and by the German Research Foundation (BB). The founders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. The authors are indebted to H. Fiedler, B. Zastrow, B. Kuhr, and V. Haensel-Bringmann for technical assistance. We thank C. Rodde, S. Piontek, M. Koelln, G. Jopp, Prof. I. Cascorbi and M. Ufer for laboratory analysis.

The manuscript was presented in part at the Annual Meeting of the Society of Neurosurgical Anesthesia and Critical Care, Orlando, FL, USA, 17th October 2008, and at the 3rd International Hypothermia Symposium, Lund, Sweden, 5th September GSK-3 2009.
Despite relevant improvements in the treatment of acute respiratory distress syndrome (ARDS) mortality remains high. The estimated annual number of deaths due to acute lung injury was calculated as 74,500 for the US in a population-based study in 2005 [1]. Mortality in severe ARDS with a high lung-injury score (>3.5) and a low oxygenation index is reported to be considerably higher and may reach more than 80% [2,3].