LeMay D R, Lu A C, Zelenock G B, D'Alecy L G
Department of Physiology and Surgery, University of Michigan Medical School, Ann Arbor 48109.
J Surg Res. 1988 Apr;44(4):352-8. doi: 10.1016/0022-4804(88)90177-1.
The effect of insulin induced hypoglycemia was evaluated in a rat aortic occlusion model of ischemic paraplegia. One hour before aortic occlusion, 200-250 g Sprague-Dawley rats received either 1 cc of saline or 0.5 units regular insulin in 1 cc saline. Rats were then anesthetized, intubated, and ventilated with halothane (1-1.5%). The aortic arch was exposed and snares were placed on the right and left subclavian arteries and the aorta distal to the left subclavian. The three vessels were occluded for 10 min. Lower extremity neurologic deficit was evaluated at 1, 4, 18, and 24 hr postocclusion based on a 15-point scale (0 = normal, 15 = severe deficit). Lower extremity neurologic deficit was significantly decreased in the insulin-treated group at 18 and 24 hr postocclusion (P = 0.005 and 0.006, respectively, Student's test). Blood glucose concentration was significantly lower at the time of occlusion in the insulin-treated group when compared to the saline-treated group (P = 0.001). We conclude that in this rat model of paraplegia, insulin induced hypoglycemia is associated with a reduction in lower extremity neurologic deficit produced by temporary aortic occlusion.
