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Am J Physiol Heart Circ Physiol 284: H2360-H2367, 2003. First published January 30, 2003; doi:10.1152/ajpheart.00899.2002
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Vol. 284, Issue 6, H2360-H2367, June 2003

Rapid modification of the glycocalyx caused by ischemia-reperfusion is inhibited by adenosine A2A receptor activation

Steven H. Platts, Joel Linden, and Brian R. Duling

Department of Molecular Physiology and Biological Physics and The Cardiovascular Research Center, University of Virginia, Charlottesville, Virginia 22908

Ischemia-reperfusion (I/R) has been shown to cause microvascular dysfunction and to alter the appearance of the glycocalyx in electron micrographs. We hypothesized that I/R injury might alter the structure and/or permeability of the glycocalyx. Prior work had shown a role for adenosine in protection from I/R injury, and, therefore, we also explored the idea that activation of the adenosine A2A receptor would attenuate I/R glycocalyx injury. Here, we report that I/R causes a rapid and dramatic decrease in the ability of the glycocalyx to exclude FITC-Dextran 70 (Dex70). Over a reperfusion period of 45 min, the glycocalyx dye exclusion zone for Dex70 decreased by one-half in capillaries and postcapillary venules, whereas the red blood cell exclusion zone was very slightly reduced in capillaries only. Pretreatment with the A2A agonist ATL-146e significantly inhibited the changes in both vessel types. The modifications of the glycocalyx appear to be an early step in the inflammatory cascade typically associated with reperfusion injury, and adenosine A2A receptor activation may play a role in protection from this injury.

endothelium; inflammation; permeability; capillary; mast cell


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