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Ann Thorac Surg 2001;72:1245-1250
© 2001 The Society of Thoracic Surgeons

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Original article: cardiovascular

Systemic adenosine A_2A agonist ameliorates ischemic reperfusion injury in the rabbit spinal cord

^a Division of Thoracic and Cardiovascular Surgery, Department of Surgery, The University of Virginia Health System, Charlottesville, Virginia, USA
^b Department of Chemistry, The University of Virginia College of Arts and Sciences, Charlottesville, Virginia, USA
^c Department of Molecular Physiology, The University of Virginia Health System, Charlottesville, Virginia, USA

Address reprint requests to Dr Kern, Department of Surgery, University of Virginia Health Sciences Center, Box 181-95, Charlottesville, VA 22908
e-mail: jak3r{at}virginia.edu

Presented at the Poster Session of the Thirty-seventh Annual Meeting of The Society of Thoracic Surgeons, New Orleans, LA, Jan 29–31, 2001.

Background. The adenosine A_2A agonist ATL-146e (4-{3-[6-Amino-9-(5-ethylcarbamoyl-3,4-dihydroxy-tetrahydro-furan-2-yl)-9H-purin-2-yl]-prop-2-ynyl}-cyclohexanecarboxylic acid methyl ester) has been shown to prevent reperfusion injury in multiple organ systems through inhibition of activated leukocyte–endothelial interaction. We hypothesized that systemic ATL-146e could reduce spinal cord reperfusion injury after aortic clamping.

Methods. Twenty-six rabbits underwent cross-clamping of the infrarenal aorta for 45 minutes. One group received intravenous ATL-146e for 3 hours during reperfusion. A second cohort received only vehicle and served as controls. Animals were assessed at 24 and 48 hours using the Tarlov (0 to 5) scoring system for hind limb function. To evaluate neuronal attrition, immunostaining of lumbar spinal cord sections was performed using anti-SMI 33 antibody against neurofilament.

Results. Systemic ATL-146e was tolerated without hemodynamic lability. Animals that received ATL-146e had significantly improved neurologic outcomes 24 and 48 hours after spinal cord ischemia (p < 0.001). There was preservation of neuronal architecture in the ventral horn of spinal cord sections from animals receiving ATL-146e compared with control animals.

Conclusions. Intravenous ATL-146e given during reperfusion is tolerated without hemodynamic lability, and results in substantially improved spinal cord function after ischemia by preservation of ventral horn neurons.

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