Postischemic hyperglycemia worsens neurologic outcome after spinal cord ischemia.
OBJECTIVE
The neurologic effect of induced hyperglycemia in the postischemic period was investigated with a rat aortic occlusion model.


METHODS
Sprague-Dawley rats weighing 200 to 350 gm were anesthetized, intubated, and ventilated with 1% to 1.5% halothane. Temperature was continuously monitored and maintained at 37 degrees +/- 0.5 degrees C. The chest was opened, the thymus excised, and the aortic arch exposed. Snares were placed around the aorta distal to the left subclavian artery and the right and left subclavian arteries. The three vessels thus isolated were occluded for 8 minutes. With snare release and withdrawal, the rats received an intraperitoneal injection of 5% dextrose in water (2 gm/kg) or an equivalent volume of 0.9% saline solution. In a second group of rats the administration of glucose or saline solution was delayed until 30 minutes after snare release. Blood samples for blood glucose determination were obtained before operation, before occlusion, immediately after occlusion, and 15, 30, 45, 60, and 240 minutes after occlusion. A neurologic deficit score was assigned at 1, 4, 18, and 24 hours after occlusion to quantify hindlimb neurologic deficit based on 15-point scale (0 = normal, 15 = severe deficit). Sham-operated rats received the same operation and injection, but the snares were only manipulated and not made occlusive.


RESULTS
The rats that were administered glucose immediately after snare release showed a statistically significant exacerbation of lower extremity neurologic deficit at 24 hours after occlusion (p < or = 0.05, Mann-Whitney U test). The sham-operated rats were normal (0 score) at 24 hours. Significant elevation of blood glucose (321 +/- 33 mg/dl) was seen in the glucose-injected rats at 15 minutes and continued for up to 4 hours after occlusion (p = 0.040 and 0.014, respectively; Student's t test).


CONCLUSIONS
Postischemic hyperglycemia immediately after a standard spinal cord ischemic stress worsens neurologic outcome.
Hemmila
M R
MR
Department of Physiology, University of Michigan Medical School, Ann Arbor 48109-0622.
Zelenock
G B
GB
D'Alecy
L G
LG
D000818:Animals; D001011:Aorta / Q000502:physiology; D001786:Blood Glucose / Q000032:analysis; D003250:Constriction; D004195:Disease Models, Animal; D005121:Extremities / Q000294:innervation / Q000503:physiopathology; D005947:Glucose / Q000008:administration & dosage; D006943:Hyperglycemia / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D007511:Ischemia / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D008297:Male; D010264:Paraplegia / Q000097:blood / Q000209:etiology / Q000503:physiopathology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013116:Spinal Cord / Q000098:blood supply*; D013348:Subclavian Artery / Q000502:physiology; D013997:Time Factors
D001786:Blood Glucose; D005947:Glucose