Paraplegia Model in the Rat: Glucose Exacerbation of Neurological Deficit
Spinal cord damage due to ischemia is a serious, underappreciated and relatively refractory problem in clinical practice. Mechanical and pharmacologic means of protecting the spinal cord from ischemic damage are relatively ineffective. Research involving fundamental mechanisms and means of prevention is hampered by a lack of reliable and reproducible animal models which appropriately mimic clinical situations. Because a new model of paraplegia in the rat has been developed, it is now possible to test specific interventions with more clinical relevance to the problem of paraplegia in humans. The goal of this study was to demonstrate the usefulness of this new rat paraplegia model by attempting to replicate previous findings that exogenous glucose administration exacerbates ischemic tissue damage, i.e. paraplegia. Age and weight matched male Sprague-Dawley rats underwent thoracotomy, ligation of the right internal thoracic artery and temporary occlusion of the aorta between the left common carotid and the left subclavian artery. Neurologic deficit scoring using standard methodology was done at 1, 4, 18 and 24 hours postocclusion. Functional deficit was also assessed by a computerized activity monitor for a 30 minute period at 1 and 18 hours postocclusion. Experimental groups received glucose (2g/kg) and were compared to rats given saline and to sham-operated (no ischemia, i.e. control) rats given glucose. Animals receiving exogenous glucose demonstrated a significant elevation in blood glucose compared to the group given saline. Neurologic deficit scoring demonstrated significant impairment in all ischemic animals compared to controls. Ischemic animals receiving glucose were significantly more impaired than ischemic animals receiving saline. These differences were noted both upon direct clinical examination and with computerized activity monitoring. Using the latter system statistical differences were detected in both total distance and number of vertical movements recorded by monitors. It is concluded that: 1) Glucose exacerbates the spinal cord injury in this model, 2) Exacerbation of neurologic deficit resulting from glucose administration can be graded and distinguished from control animals using an experimenter-performed neurologic scoring, 3) Computerized activity monitoring correlates with the experimenter-performed neurologic scoring.