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

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...

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Bibliographic Details
Published in:American journal of physiology. Heart and circulatory physiology 2003-06, Vol.284 (6), p.H2360-H2367
Main Authors: Platts, Steven H, Linden, Joel, Duling, Brian R
Format: Article
Language:English
Subjects:
Animals
Arterioles - pathology
Biotransformation - physiology
Capillaries - pathology
Cyclohexanecarboxylic Acids - pharmacology
Erythrocytes - physiology
Glycocalyx - pathology
Male
Mice
Mice, Inbred C57BL
Muscle, Skeletal - pathology
Purinergic P1 Receptor Agonists
Purinergic P1 Receptor Antagonists
Purines - pharmacology
Receptor, Adenosine A2A
Reperfusion Injury - pathology
Triazines - pharmacology
Triazoles - pharmacology
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Summary: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 A 2A 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 A 2A 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 A 2A receptor activation may play a role in protection from this injury. endothelium; inflammation; permeability; capillary; mast cell
ISSN:0363-6135
1522-1539
DOI:10.1152/ajpheart.00899.2002