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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: Exogenous nitric oxide requires an endothelial glycocalyx to prevent postischemic coronary vascular leak in guinea pig hearts. | Available online http ccforum.eom content 1 2 3 R73 Research Exogenous nitric oxide requires an endothelial glycocalyx to prevent postischemic coronary vascular leak in guinea pig hearts Dirk Bruegger1 Markus Rehm1 Matthias Jacob1 Daniel Chappell1 Mechthild Stoeckelhuber2 Ulrich Welsch2 Peter Conzen1 and Bernhard F Becker3 Open Access 1Clinic of Anesthesiology Ludwig-Maximilians-University Marchioninistrasse 15 81377 Munich Germany 2Department of Anatomy Ludwig-Maximilians-University Pettenkoferstrasse 11 80336 Munich Germany 3Department of Physiology Ludwig-Maximilians-University Pettenkoferstrasse 12 80336 Munich Germany Corresponding author Dirk Bruegger dirk.bruegger@med.uni-muenchen.de Received 14 Jan 2008 Revisions requested 15 Feb 2008 Revisions received 19 Mar 2008 Accepted 2 Jun 2008 Published 2 Jun 2008 Critical Care 2008 12 R73 doi 10.1186 cc6913 This article is online at http ccforum.com content 12 3 R73 2008 Bruegger et al. licensee BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License http creativecommons.org licenses by 2.0 which permits unrestricted use distribution and reproduction in any medium provided the original work is properly cited. Abstract Introduction Postisehemie injury to the coronary vascular endothelium in particular to the endothelial glycocalyx may provoke fluid extravasation. Shedding of the glycocalyx is triggered by redox stress encountered during reperfusion and should be alleviated by the radical scavenger nitric oxide NO . The objective of this study was to investigate the effect of exogenous administration of NO during reperfusion on both coronary endothelial glycocalyx and vascular integrity. Methods Isolated guinea pig hearts were subjected to 15 minutes of warm global ischemia followed by 20 minutes of reperfusion in the absence Control group and presence NO group of 4 pM NO. In further experiments the endothelial glycocalyx was enzymatically degraded by
