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Preliminary report of an enoxaparin dose protocol based on anti-Xa activity in continuous renal replacement therapy

Critical Care
Springer (Biomed Central Ltd.)
Publication Date
DOI: 10.1186/cc5843
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S1 Available online Critical Care Volume 11 Suppl 3, 2007 Fourth International Symposium on Intensive Care and Emergency Medicine for Latin America São Paulo, Brazil, 20–23 June 2007 Published online: 19 June 2007 These abstracts are online at © 2007 BioMed Central Ltd Basic science P1 Platelet-derived exosomes are redox signaling particles MH Gambim1, AO Carmo2, L Marti2, S Veríssimo-Filho1, LR Lopes1, M Janiszewski1,2 1Faculdade de Medicina and Instituto de Ciências Biomédicas, University of São Paulo – SP, Brazil; 2Instituto Israelita de Ensino e Pesquisa, Albert Einstein Hospital, São Paulo – SP, Brazil Critical Care 2007, 11(Suppl 3):P1 (doi: 10.1186/cc5788) Sepsis, the body’s response to infection, is associated with extremely high mortality rates. Why a protective mechanism turns into a deadly clinical picture is a matter of debate, and goes largely unexplained. In previous work we demonstrated that platelet-derived microparticles (MP) can induce endothelial and vascular smooth muscle cell apoptosis in septic patients through NADPH oxidase- dependent superoxide release [1]. In this work we sought to create a model for ex vivo generation of septic-like MP and to identify the pathways responsible for MP free radical release and effects. Septic shock is a condition related to the generation of high amounts of thrombin, TNFα and nitrogen reactive species. Human platelets exposed to the NO donors diethylamine-NONOate (0.5 mM) and nitroprusside (2 mM) for 20 minutes generated MP similar to those found in the blood of septic shock patients. Flow cytometry and western blot analysis of those MP, like their septic counterparts, revealed exposure of the tetraspanin markers CD9, CD63, and CD81, but little phosphatidylserine. Such a membrane exposure, associated with their size, characterizes them as exosomes. Furthermore, we identified the Nox2 and p22phox NADPH oxidase subunits and the inducible isoform of NO sy

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