LeMay D R, Neal S, Neal S, Zelenock G B, D'Alecy L G
Department of Physiology and Surgery, University of Michigan Medical School, Ann Arbor.
J Vasc Surg. 1987 Oct;6(4):383-90.
Spinal cord damage caused by ischemia is a serious, underappreciated, and relatively refractory problem in clinical practice. Research is hampered by a lack of experimental models that appropriately mimic clinical situations. A new model of paraplegia in the rat is presented and evaluated by standard neurologic deficit scoring (1, 4, 18, and 24 hours after occlusion) and by computerized activity monitoring (1 and 18 hours after occlusion). Rats underwent temporary occlusion of the thoracic aorta for 10, 15, or 20 minutes. Experimental groups received glucose (2 gm/kg) and demonstrated a significant elevation in blood glucose (p = 0.001) and were significantly more neurologically impaired at all four time periods (p less than or equal to 0.005) than the ischemic control group, which received equivalent volumes of normal saline solution. Significant differences in neurologic deficit were noted with direct clinical examination and computerized activity monitoring. With the use of the latter system, statistical differences were detected in total distance traveled and number of vertical movements. We conclude the following: (1) Paraplegia is reliably and reproducibly achieved in this rat model; (2) because of the rat's more extensive behavioral repertoire when compared with other models of spinal ischemia (e.g., rabbit), more end points can be monitored and more subtle behavioral deficits discerned; (3) computerized activity monitoring can distinguish varying degrees of neurologic deficit and correlates with clinical neurologic deficit scoring; and (4) glucose exacerbates paraplegia in this model.
