The influence of dextrose administration on neurologic outcome after temporary spinal cord ischemia in the rabbit

Abstract

The influence of dextrose administration on neurologic outcome after temporary spinal cord ischemia was examined in New Zealand white rabbits. Spinal cord ischemia was produced by infrarenal balloon occlusion of the aorta in unanesthetized animals. Animals were observed for 3 days for neurologic evaluation. Fasted animals received intravenous dextrose, 0.5 g·kg-1, or placebo before a period spinal cord ischemia. The dextrose was administered as either a bolus of a 50% solution (D50) 15 min before ischemia or as an infusion of a 5% solution (D5W) over 90 min before ischemia. With either mode of administration, preocclusion plasma glucose level was moderately increased as compared with that in animals that received lactated Ringer's solution in equivalent volume, i.e., for the D50 bolus: 291±82 (SD) versus 166±67 mg·dl-1 (P<0.005); and for D5W infusion: 177±38 versus 137±13 mg·dl-1 (P<0.01). With either mode of administration, neurologic outcome was poorer (P<0.025) at 72 h in the animals that had received dextrose. For example, of the 10 animals that received D5W by infusion, nine were paraplegic (unable to walk) 72 h after ischemia, whereas only three of 10 control animals were paraplegic. The adverse effect of an increased blood glucose level has been demonstrated previously for cerebral ischemia. The present results are the first demonstration that increased plasma glucose may result in a worsened neurologic outcome after spinal cord ischemia. Further, they indicate that, in rabbits, the threshold for this effect is low, i.e., dextrose administration sufficient to produce a mean preischemic plasma glucose increase of 40 mg·dl-1 was sufficient to result in an increased frequency of postischemic paraplegia.