Pulmonary vascular permeability changes in an ovine model of methicillin-resistant Staphylococcus aureus sepsis 英文参考文献.docVIP

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Pulmonary vascular permeability changes in an ovine model of methicillin-resistant Staphylococcus aureus sepsis 英文参考文献.doc

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Pulmonary vascular permeability changes in an ovine model of methicillin-resistant Staphylococcus aureus sepsis 英文参考文献

Available online /content/13/1/R19 Research Open Access Vol 13 No 1 Pulmonary vascular permeability changes in an ovine model of methicillin-resistant Staphylococcus aureus sepsis Collette C Jonkam1, Kamna Bansal1, Daniel L Traber1, Atsumori Hamahata1, Marc O Maybauer1, Dirk M Maybauer1, Robert A Cox2, Matthias Lange1, Rhykka L Connelly1, Lillian D Traber1, Clarisse D Djukom1, John R Salsbury1, David N Herndon3 and Perenlei Enkhbaatar1 1Department of Anesthesiology, The University of Texas Medical Branch and Shriners Hospital for Children, 601 Harborside Drive, Galveston, TX 77555-1102, USA 2Department of Pathology, The University of Texas Medical Branch and Shriners Hospital for Children, 301 University Blvd, Galveston, TX 77555, USA 3Department of Surgery, The University of Texas Medical Branch and Shriners Hospital for Children, 301 University Blvd, Galveston, TX 77555, USA Corresponding author: Collette C Jonkam, ccjonkam@ Received: 2 Dec 2008 Revisions requested: 12 Jan 2009 Revisions received: 3 Feb 2009 Accepted: 17 Feb 2009 Published: 17 Feb 2009 Critical Care 2009, 13:R19 (doi:10.1186/cc7720) This article is online at: /content/13/1/R19 ? 2009 Jonkam et al.; licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Introduction Endothelial dysfunction is a hallmark of sepsis, associated with lung transvascular fluid flux and pulmonary dysfunction in septic patients. We tested the hypothesis that methicillin-resistant Staphylococcus aureus (MRSA) sepsis following smoke inhalation increases pulmonary transvascular fluid flux via excessive nitric oxide (NO) production. gas exchange and significantly increased lung lymph flow, permeability index and bloodless wet-to-dry weight-ratio (W/D rati