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Am J Physiol Heart Circ Physiol 281: H67-H74, 2001;
0363-6135/01 $5.00
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Vol. 281, Issue 1, H67-H74, July 2001

Selective A2A adenosine receptor activation reduces skin pressure ulcer formation and inflammation

Shayn M. Peirce1, Thomas C. Skalak1, Jayson M. Rieger2, Timothy L. Macdonald2, and Joel Linden3

Departments of 1 Biomedical Engineering, 2 Chemistry, and 3 Cardiovascular Medicine, University of Virginia, Charlottesville, Virginia 22908

Activation of A2A adenosine receptors (A2A-AR) by ATL-146e (formerly DWH-146e) prevents inflammatory cell activation and adhesion. Recurrent ischemia-reperfusion (I/R) of the skin results in pressure ulcer formation, a major clinical problem. ATL-146e was evaluated in a novel reproducible rat model of pressure ulcer. A 9-cm2 region of dorsal rat skin was cyclically compressed at 50 mmHg using a surgically implanted metal plate and an overlying magnet to generate reproducible tissue necrosis. Osmotic minipumps were implanted into 24 rats divided into four equal groups to infuse vehicle (control), ATL-146e (0.004 µg · kg-1 · min-1), ATL-146e plus an equimolar concentration of A2A antagonist, ZM-241385, or ZM-241385 alone. Each group received 10 I/R cycles. In non-I/R-treated skin, ATL-146e has no effect on blood flow. I/R-treated skin of the ATL-146e group compared with the vehicle group had 65% less necrotic area, 31% less inhibition of average skin blood flow, and fewer extravasated leukocytes (23 ± 3 vs. 49 ± 6 per 500 µm2). These data suggest that ATL-146e, acting via an A2A-AR, reduces leukocyte infiltration and is a potent prophylactic for I/R injury in skin.

ischemia-reperfusion; leukocyte extravasation; magnetic force; skin necrosis


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