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OtherCARDIOVASCULAR PHARMACOLOGY

Adenosine A2 Receptor Activation Attenuates Reperfusion Injury by Inhibiting Neutrophil Accumulation, Superoxide Generation and Coronary Endothelial Adherence

James E. Jordan, Zhi-Qing Zhao, Hiroki Sato, Spencer Taft and Jakob Vinten-Johansen
Journal of Pharmacology and Experimental Therapeutics January 1997, 280 (1) 301-309;
James E. Jordan
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Zhi-Qing Zhao
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Hiroki Sato
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Spencer Taft
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Jakob Vinten-Johansen
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Abstract

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 ± 4.1vs. 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). Inin 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 (cytochromec 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.

Footnotes

  • Send reprint requests to: Jakob Vinten-Johansen, Ph.D., Department of Cardiothoracic Surgery, Cardiothoracic Research Laboratory, Carlyle Fraser Heart Center, Peachtree St., N. E., Atlanta, GA 30365-2225.

  • ↵1 This study was supported by grants from the National Institutes of Heath (Grant HL46179) and from the American Heart Association, North Carolina Affiliate.

  • Abbreviations:
    AAR
    area at risk
    CK
    creatine kinase
    EDSL
    end-diastolic segment length
    ESSL
    end-systolic segment length
    LAD
    left anterior descending coronary artery
    LV
    left ventricle
    MAP
    mean aortic pressure
    MPO
    myeloperoxidase
    PAF
    platelet-activating factor
    PBS
    phosphate-buffered saline
    PMN
    polymorphonuclear leukocyte
    PRP
    pressure-rate product
    SOD
    superoxide dismutase
    • Received February 8, 1996.
    • Accepted September 25, 1996.
  • The American Society for Pharmacology and Experimental Therapeutics
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Journal of Pharmacology and Experimental Therapeutics
Vol. 280, Issue 1
1 Jan 1997
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OtherCARDIOVASCULAR PHARMACOLOGY

Adenosine A2 Receptor Activation Attenuates Reperfusion Injury by Inhibiting Neutrophil Accumulation, Superoxide Generation and Coronary Endothelial Adherence

James E. Jordan, Zhi-Qing Zhao, Hiroki Sato, Spencer Taft and Jakob Vinten-Johansen
Journal of Pharmacology and Experimental Therapeutics January 1, 1997, 280 (1) 301-309;

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OtherCARDIOVASCULAR PHARMACOLOGY

Adenosine A2 Receptor Activation Attenuates Reperfusion Injury by Inhibiting Neutrophil Accumulation, Superoxide Generation and Coronary Endothelial Adherence

James E. Jordan, Zhi-Qing Zhao, Hiroki Sato, Spencer Taft and Jakob Vinten-Johansen
Journal of Pharmacology and Experimental Therapeutics January 1, 1997, 280 (1) 301-309;
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