Lakis2, O Livaditi1, E GiamarellosBourboulis3, C Sotiropoulou1, A Koutsoukou4, I Dimopoulou2, A Armaganidis2, C Roussos4,

Lakis2, O Livaditi1, E GiamarellosBourboulis3, C Sotiropoulou1, A Koutsoukou4, I Dimopoulou2, A Armaganidis2, C Roussos4, N Marczin5, A Kotanidou4, S Orfanos2 1University of Athens, Greece; 2Attikon Hospital, 2nd Critical Care Department, Haidari (Athens), Greece; 3Attikon Hospital, 4th Department of Medicine, Haidari (Athens), Greece; 4Evangelismos Hospital, Athens, Greece; 5Imperial College London, UK Critical Care 2007, 11(Suppl 2):P20 (doi: 10.1186/cc5180) Introduction Mechanical ventilation may induce lung Src-l1 price injury in patients with normal lungs. Application of PEEP appears protective. Lung injury is associated with the production and release of inflammatory mediators. Such mediators have been identified in patients’ exhaled breath condensate (EBC) in various lungFigure 1 (abstract P21)pathologies. In this study we identified EBC inflammatory markers in 27 mechanically ventilated brain-injured subjects with neither acute lung injury (ALI) nor sepsis. Methods Patients were ventilated with 8 ml/kg tidal volume and were put either on PEEP = 0 (ZEEP, n = 12) or 8 cmH2O (PEEP, n = 15). EBC was collected using the RTube device (Respiratory Research Inc., Charlottesville, PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/20799915 VA, US) on the first, third, and fifth day of mechanical ventilation, and pH, IL-10, IL-1, IL-6, IL-8, IL-12p70 and TNF were measured. Applying mixed effects models, we further investigated potential relationships of the above EBC markers with indices of: i, lung injury (LIS score, PaO2/FiO2, detected pathologies on lung CT); ii, brain injury (ICP, CPP, GCS, serum (s) S100 protein, pentothal and mannitol administration); iii, endothelial injury (sICAM-1, sVCAM-1, von Willebrand factor antigen); iv, systemic inflammation (temperature, leukocyte counts and neutrophil counts in blood, albumin, soluble triggering receptor expressed on myeloid cells (sTREM), CRP, procalcitonin (PCT) and all above-mentioned cytokines in serum or plasma); and v, disease severity (APACHE II score, 24 hour ICU trauma score, presence of SIRS, mean arterial pressure). Results No significant differences in EBC measurements were observed between the two groups except a time-dependent decrease in IL-10 (P < 0.05, by ANOVA) in the PEEP group. EBC pH and IL-10 showed no significant relationships (mixed effects models) with any parameter measured. All other EBC cytokines were inversely related to sTREM levels. Additional significant relationships were obtained between individual EBC cytokines and sIL-8 (IL-8, IL-12p70, TNF), sIL-6 (IL-1), PCT (IL-1, IL-12p70), the existence of SIRS (IL6, IL-8), sVCAM-1 (IL-6), and pentothal administration (IL-1). Conclusion In our population of mechanically ventilated, braininjured patients with no ALI, ZEEP or applied PEEP did not induce detectable changes in most lung inflammatory mediators in EBC; the latter appear mostly related to markers of systemic inflammation (especially sTREM-1) rather than to indices of brain and endothelial injury.P21 Reduced local inflammatory reactivity in septic patients compared with healthy controlsD Ikeoka1, C Pachler1, S Korsatko1, M Bodenlenz2, J Mader1, H Weinhandl1, A Plasnik1, M Suppan1, K Smolle1, J Plank1, T Pieber1, M Ellmerer1 1Medical University Graz, Austria; 2Joanneum Research, Graz, Austria Critical Care 2007, 11(Suppl 2):P21 (doi: 10.1186/cc5181) Introduction The aim of this study was to access the local inflammatory reactivity by measurement of the cytokine responseSAvailable online http://ccforum.com/supplements/11/Safter c.