Background and purpose: Spinal cord ischemic injury (SCII) with resulting paralysis is a major cause of morbidity after operations on the thoracic aorta. Since the vascular supply to the spinal cord is similar in rats and humans, the rat appears important for studies of mechanisms of injury and development of therapeutic strategies to avoid this complication.
Methods: In group A rats, we induced SCII using a previously described method, by occluding the descending thoracic aorta for 15, 20, 24, or 30 minutes with the inflated balloon of a 2F Fogarty catheter inserted through the femoral artery. In group B, the catheter was inserted through the left common carotid artery, and the aorta was occluded just distal to the carotid origin for 20 minutes. In group C, in addition to the procedure described for group B, hypovolemia was induced during a 12-minute period of aortic occlusion by equilibrating the left femoral artery pressure to the atmospheric pressure. The motor function of the hind limbs and the associated spinal cord histopathology were studied.
Results: At 96 hours, 9 of 10 rats in group C were paraplegic. This rate was significantly higher than that of group A (1 of 21, P = .00000) or group B (4 of 10, P < .03). In all groups, the histopathological changes became more severe from the rostral to the caudal direction along the spinal cord and from the peripheral to the central location in transverse sections.
Conclusions: The combination of aortic arch occlusion with induced hypovolemia resulted in a reproducible model of SCII in rats.