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Am J Physiol Heart Circ Physiol (January 30, 2003). doi:10.1152/ajpheart.00899.2002
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Submitted on October 16, 2002
Accepted on January 22, 2003

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

Steven H. Platts1, Joel Linden1, and Brian R. Duling1*

1 Department of Molecular Physiology and Biological Physics, University of Virginia, Charlottesville, VA, USA

* To whom correspondence should be addressed. E-mail: brd{at}virginia.edu.

Ischemia/reperfusion (I/R) has been shown to cause microvascular dysfunction and to alter the appearance of the glycocalyx in electronmicrographs. 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. Over a reperfusion period of 45 minutes, the glycocalyx dye exclusion zone for Dex70 decreases by half in capillaries and post-capillary venules, while the red cell exclusion zone is 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 A2A activation may play a role in protection from this injury.




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