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J Thorac Cardiovasc Surg 2002;124:973-978
© 2002 The American Association for Thoracic Surgery

Cardiothoracic Transplantation (TX)

Adenosine A_2A receptor activation decreases reperfusion injury associated with high-flow reperfusion

From the Department of Thoracic and Cardiovascular Surgery, University of Virginia Health Sciences Center, Charlottesville, Va.

Supported by the National Institutes of Health (NIH) under R01 grant HL56093-03, National Research Service Award F32 grant HL10248-01, and cooperative agreement U54 HD28934 as part of the Specialized Cooperative Centers Program in Reproduction Research.

Read at the Eighty-first Annual Meeting of The American Association for Thoracic Surgery, San Diego, Calif, May 6-9, 2001.

Received for publication May 15, 2001. Revisions requested June 28, 2001; revisions received Dec 27, 2001; revisions requested Feb 13, 2002; revisions received Feb 18, 2002. Accepted for publication Feb 21, 2002. Address for reprints: Steven M. Fiser, MD, Department of Thoracic and Cardiovascular Surgery, University of Virginia Health Sciences Center, PO Box 801359, MR4 Building, Room 3111, Charlottesville, VA 22908 (E-mail: smf9e{at}virginia.edu).

Introduction: High pulmonary artery flow rates can result in severe reperfusion injury after lung transplantation. Our hypothesis was that selective activation of the adenosine A_2A receptor with a highly specific analog (ATL-146e) would inhibit leukocyte activation and decrease reperfusion injury after high-flow reperfusion.
Methods: Using our isolated, ventilated, blood-perfused rabbit lung model, all groups (n = 8 per group) underwent lung harvest, 4 hours of cold storage, and blood reperfusion for 30 minutes. Measurements of pulmonary artery pressure (in millimeters of mercury), arterial oxygenation (in millimeters of mercury), myeloperoxidase, peak inspiratory pressure, and wet/dry weight ratio were obtained. Groups 1 (high flow) and 2 (high flow ATL-146e) underwent reperfusion at 120 mL/min for 30 minutes. Groups 3 (controlled high flow) and 4 (controlled high flow ATL-146e) underwent controlled reperfusion with an initial reperfusion of 60 mL/min for the first 5 minutes, followed by a rate of 120 mL/min for 25 minutes. During reperfusion, groups 2 and 4 received ATL-146e at 4 µg · kg^-1 · min^-1.
Results: ATL-146e significantly improved lung physiologic measurements under both high-flow (group 1 vs group 2) and controlled high-flow (group 3 vs group 4) conditions after 30 minutes.
Conclusions: The adenosine A_2A receptor analogue ATL-146e significantly decreases the severity of reperfusion injury in the setting of both high-flow and controlled high-flow reperfusion.

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