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J Thorac Cardiovasc Surg 2000;119:588-595
© 2000 Mosby, Inc.


CARDIOPULMONARY SUPPORT AND PHYSIOLOGY

HYPOTHERMIC RETROGRADE VENOUS PERFUSION WITH ADENOSINE COOLS THE SPINAL CORD AND REDUCES THE RISK OF PARAPLEGIA AFTER THORACIC AORTIC CLAMPING

Scott D. Ross, MD, John A. Kern, MD, James J. Gangemi, MD, Char R. St Laurent, REEGT, Kimberly S. Shockey, MS, Irving L. Kron, MD, Curtis G. Tribble, MD

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

Address for reprints: Curtis G. Tribble, MD, Department of Surgery, Division of Thoracic and Cardiovascular Surgery, University of Virginia Health Sciences Center, Box 3111, MR4 Building, Charlottesville, VA 22908 (E-mail: cgt2e{at}aol.com ).

Objective: We evaluated the utility of retrograde venous perfusion to cool the spinal cord and protect neurologic function during aortic clamping. We hypothesized that hypothermic adenosine would preserve the spinal cord during ischemia.
Methods: Six swine (group I) underwent thoracic aortic occlusion for 30 minutes at normothermia. Group II animals underwent spinal cooling by retrograde perfusion of the paravertebral veins with hypothermic (4°C) saline solution during aortic occlusion. The spinal cords of group III animals were cooled with a hypothermic adenosine solution in a similar fashion. Intrathecal temperature was monitored and somatosensory evoked potentials assessed the functional status of spinal pathways.
Results: Spinal cooling without systemic hypothermia significantly improved neurologic Tarlov scores in group III (4.8 ± 0.2) and group II (3.8 ± 0.4) when compared with group I scores (1.3 ± 0.6) (P < .001). Furthermore, 5 of the 6 animals in group III displayed completely normal neurologic function, whereas only one animal in group II and no animals in group I did (P = .005). Somatosensory evoked potentials were lost 10.6 ± 1.4 minutes after ischemia in group I. In contrast, spinal cooling caused rapid cessation of neural transmission with loss of somatosensory evoked potentials at 6.9 ± 1.2 minutes in group II and 7.0 ± 0.8 minutes in group III (P = .06). Somatosensory evoked potential amplitudes returned to 85% of baseline in group III and 90% of baseline in group II compared with only 10% of baseline in group I (P = .01).
Conclusions: We conclude that retrograde cooling of the spinal cord is possible and protects against ischemic injury and that adenosine enhances this effect. The efficacy of this method may be at least partly attributed to a more rapid reduction in metabolic and electrical activity of the spinal cord during ischemia.




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