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J Thorac Cardiovasc Surg 2004;128:925-932
© 2004 The American Association for Thoracic Surgery

Surgery for Acquired Cardiovascular Disease

The evolution of ischemic spinal cord injury in function, cytoarchitecture, and inflammation and the effects of adenosine A_2A receptor activation

^a Department of Surgery, University of Virginia Health System, Charlottesville, Va
^b Department of Neuroscience, University of Virginia Health System, Charlottesville, Va
^c Department of Cardiovascular Research Center, University of Virginia Health System, Charlottesville, Va

Read at the Eighty-fourth Annual Meeting of The American Association for Thoracic Surgery, Toronto, Ontario, Canada, April 25-28, 2004.

Received for publication April 23, 2004; revisions received August 8, 2004; accepted for publication August 10, 2004.

^* Address for reprints: T. Brett Reece, MD, Department of Surgery, University of Virginia Health System, PO Box 801359, MR4 Building, Room 3116, Charlottesville, VA 22908 (E-mail: tbr5q{at}virginia.edu).

OBJECTIVE: Spinal cord ischemia/reperfusion injury involves multiple factors that may be modulated by adenosine A_2A receptor activation. This study defines injury progression in terms of function, cytoarchitecture, and inflammation and assesses whether adenosine A_2A receptor activation by ATL-146e limits injury progression.

METHODS: Mature swine were divided into 3 groups: sham thoracotomy, IR (30 minutes of ischemia followed by reperfusion), and ATL (ischemia/reperfusion with ATL-146e administration for the first 3 hours of reperfusion). Subgroups were killed at 0, 3, 6, 12, 24, and 48 hours after reperfusion. Function was followed up with Tarlov scores. Spinal cord tissue was evaluated for neuronal viability, microtubule-associated protein–2 immunohistochemistry, and neutrophil sequestration (myeloperoxidase assay). Spinal cord tissue, cerebrospinal fluid, and serum were evaluated for tumor necrosis factor- by enzyme-linked immunosorbent assay.

RESULTS: Function was significantly impaired at 24, 36, and 48 hours in the IR group compared with the sham and ATL groups (P < .05). Neuronal viability and microtubule-associated protein–2 staining were significantly preserved in the sham and ATL groups compared with the IR group at 24 and 48 hours (P < .05). Spinal cord myeloperoxidase levels were significantly higher in the IR group than in the sham and ATL groups at 24 and 48 hours. Although negligible in serum and cerebrospinal fluid, tumor necrosis factor- levels in the spinal cord peaked significantly higher in the IR group compared with the sham and ATL groups at 6 and 24 hours (P < .05).

CONCLUSIONS: Spinal cord ischemia/reperfusion induced changes in neutrophil sequestration, microtubule-associated protein–2 expression, and neuronal viability within 24 hours of reperfusion. Spinal cord tumor necrosis factor- increased significantly by 6 to 12 hours after reperfusion. Adenosine A_2A receptor activation attenuates spinal cord inflammation, which may be critical for the preservation of neuronal function and cytoarchitecture after ischemia/reperfusion.

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