The effect of hyperglycemia on cerebral metabolism during hypoxia-ischemia in the immature rat

Unlike adults, hyperglycemia with circulating glucose concentrations of 25-35 mM/L protects the immature brain from hypoxic-ischemic damage. To ascertain the effect of hyperglycemia on cerebral oxidative metabolism during the course of hypoxia-ischemia, 7-day postnatal rats underwent unilateral common carotid artery ligation followed by exposure to 8% O-2 for 2 h at 37 degrees C. Experimental animals received 0.2 cc s.c. 50% glucose at the onset of hypoxia-ischemia. and 0.15 cc 25% glucose 1 h later to maintain blood glucose concentrations at 20-25 mM/L for 2 h. Control rat pups received equivalent concentrations or volumes of either mannitol or 1 N saline at the same intervals. The cerebral metabolic rate for glucose (CMR(glc)) increased from 7.1 (control) to 20.2 mu mol 100 g(-1) min(-1) in hyperglycemic rats during the first hour of hypoxia-ischemia, 79 and 35% greater than the rates for saline- and mannitol-injected animals at the same interval, respectively (p < 0.01). Brain intracellular glucose concentrations were 5.2 and 3.0 mM/kg in the hyperglycemic rat pups at 1 and 2 h of hypoxia-ischemia.