Spinal
ischemia with resultant cord
infarction is a catastrophic complication of
surgical procedures involving the thoracoabdominal aorta. A rabbit spinal
ischemia model was used to test if
glucose administration would increase
neurologic deficit of the lower extremity. Rabbits (2 to 3 kg), anesthesized with
halothane, had a snare occluder placed around the aorta just below the left renal artery. After a 2-hour recovery, the aorta was occluded for 15 minutes. Before occlusion animals received an
intraperitoneal injection of isotonic
glucose (2 gm/kg; n = 11), isotonic
mannitol (2 gm/kg; n = 3), or an equal volume of
saline solution (n = 11). Four
sham-operated animals received
glucose and an identical
surgical procedure, but the aorta was not occluded. Average
blood glucose level at the time of occlusion for the
glucose group was 249 +/- 15 versus 156 +/- 6 for the control group (p less than 0.01). At 1, 4, 18, and 24 hours, a neurologic impairment score (1 = normal, 2 = partial impairment, 3 = complete impairment) was assigned. At 4, 18, and 24 hours, the
glucose group had significantly greater neurologic impairment than did control groups (p less than 0.02).
Glucose administration had an adverse effect in a controlled and highly reproducible model of
spinal cord ischemia. Exogenous
glucose administration should potentially be avoided during complex aortic reconstruction.