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J Thorac Cardiovasc Surg 1994;107:536-0542
© 1994 Mosby, Inc.


Cardiopulmonary Bypass, Myocardial Management, and Support Techniques

Complete prevention of postischemic spinal cord injury by means of regional infusion with hypothermic saline and adenosine

Jeffrey A. Herold, MD (by invitation)


Roanoke, Va.

Irving L. Kron, MD, Scott E. Langenburg, MD (by invitation), Lorne H. Blackbourne, MD (by invitation), Curtis G. Tribble, MD (by invitation)


Charlottesville, Va.

From the Department of Surgery, University of Virginia Health Sciences Center, Charlottesville, Va., and Roanoke Memorial Hospital,a Roanoke, Va.

Address for reprints: Curtis G. Tribble, MD, Department of Surgery, Box181, University of Virginia Health Science Center, Charlottesville, VA 22908.

Abstract

Spinal cord injury after operations on the descending thoracic and thoracoabdominal aorta remains a persistent clinical problem. Previous attempts to decrease the risk of this devastating complication by lowering the rate of metabolism of the spinal cord have met with varying success. We hypothesized that the tolerance of the spinal cord to an ischemic insult could be improved by means of adenosine. Twenty New Zealand white rabbits underwent 40 minutes of isolated infrarenal aortic occlusion after heparin anticoagulation. Clamps were placed both below the left renal vein and above the aortic bifurcation. In 10 rabbits (group A), a bolus of adenosine (100 mg) was infused into the isolated aortic segment immediately after crossclamping and this bolus was followed by a flush of hypothermic saline (8° C, 30 ml/kg) over the first 10 minutes of ischemia. In one control group of five animals (group B), the descending infrarenal aorta was crossclamped without infusion of adenosine or saline. In another control group of five animals (group C), the aortic segment was flushed with normothermic saline (37 ° C) in a fashion identical to that of the study group. The aortic clamps were removed after 40 minutes, the abdomen was closed, and the animals were allowed to recover from anesthesia. Spinal cord function was assessed 12, 24, 48, 72, and 96 hours after operation by the Tarlov scale. All animals were put to death at 96 hours after operation and spinal cords were harvested for histologic analysis. The spinal cord function of all group A animals was fully intact with Tarlov scores of 5; group B and group C animals were all paraplegic with Tarlov scores of 0 (p < 0.001, general linear models analysis of variance). Histologic examination of spinal cords from group A rabbits revealed no evidence of cord injury, whereas spinal cords from groups B and C had evidence of extensive cord injury with central gray necrosis, axonal swelling, dissolution of Nissl substance, and astrocyte and macrophage infiltration. Regional infusion of the crossclamped infrarenal rabbit aorta with hypothermic saline and adenosine completely prevented paraplegia in our model despite a 40-minute ischemic insult. (J THORAC CARDIOVASC SURG 1994;107:536-42)




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