Báo cáo y học: "Pulmonary vascular permeability changes in an ovine model of methicillin-resistant Staphylococcus aureus sepsis"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Pulmonary vascular permeability changes in an ovine model of methicillin-resistant Staphylococcus aureus sepsis. | Available online http content 13 1 R19 Open Access Research Pulmonary vascular permeability changes in an ovine model of methicillin-resistant Staphylococcus aureus sepsis Collette C Jonkam1 Kamna Bansal1 Daniel LTraber1 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 Department of Anesthesiology The University of Texas Medical Branch and Shriners Hospital for Children 601 Harborside Drive Galveston TX 77555-1102 USA department of Pathology The University of Texas Medical Branch and Shriners Hospital for Children 301 University Blvd Galveston TX 77555 USA department 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 cc7720 This article is online at http 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 http licenses by 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. Methods Ewes were chronically instrumented and randomised into either a control or MRSA sepsis MRSA and smoke inhalation group. Results Pulmonary function remained stable in

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