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Vol. 280, Issue 1, 301-309, 1997
Bowman Gray School of Medicine, Department of Physiology and
Pharmacology, Department of Cardiothoracic Surgery, Research
Laboratory, Winston-Salem, North Carolina
This study tests the hypothesis that adenosine A2 receptor
activation reduces reperfusion injury by inhibiting neutrophils in a
canine model of ischemia and reperfusion. In 16 anesthetized, open-chest dogs, the left anterior descending coronary artery was
ligated for 60 min and reperfused for 3 hr. An intracoronary infusion
of either the selective adenosine A2 agonist CGS-21680 at
0.2 µg/kg/min (n = 8) or vehicle
(n = 8) was started 5 min before reperfusion and
discontinued after 60 min. The area at risk was comparable between
vehicle-treated and CGS-21680-treated groups (39.6 ± 4.1 vs. 37.1 ± 2.5% of left ventricle). Infarction size, determined with triphenyltetrazolium chloride, was smaller in the
CGS-21680-treated group than in the vehicle-treated group (15.4 ± 2.9 vs. 29.8 ± 2.3% of area at risk, P < .05 vs. vehicle-treated group). CGS-21680 significantly
reduced neutrophil accumulation (myeloperoxidase activity) in the
nonnecrotic area at risk tissue, compared with the vehicle-treated
group (2.12 ± 0.5 vs. 6.47 ± 0.6 U/g of
tissue, P < .05 vs. vehicle-treated group). In
in vitro studies, CGS-21680 reduced platelet-activating
factor (PAF)-activated canine neutrophil adherence to the endothelial
surface of normal homologous coronary artery segments. Compared with
PAF-stimulated neutrophils (188.4 ± 9.4 adhered
neutrophils/mm2), CGS-21680 reduced adherence close to
base-line levels (46.6 ± 5.8 adhered neutrophils/mm2)
at concentrations of 10 µM (65.6 ± 8.2 adhered
neutrophils/mm2, P < .05 vs.
PAF-stimulated group) and 50 µM (56.6 ± 4.6 adhered neutrophils/mm2, P < .05 vs.
PAF-stimulated group). Superoxide anion production (cytochrome
c reduction) by activated neutrophils was reduced by
CGS-21680 from 33.8 ± 5.0 to 8.9 ± 3.6 nmol/5 min/5 × 106 cells (P < .05 vs. PAF-stimulated
group). We conclude that specific A2 receptor stimulation
with CGS-21680 at reflow reduces reperfusion injury by inhibiting
neutrophil-related processes.
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