1712 GLUCOSE SUPPLEMENTATION DOES NOT ACCENTUATE HYPOXICISCHEMIC BRAIN DAMAGE IN IMMATURE RATS: BIOCHEMICAL MECHANISMS

Abstract

Previous investigations from our laboratory have shown that hyperglycemia during the course of hypoxia-ischemia (H-I) does not increase brain damage in immature animals as occurs in adults (Voorhies et al 1982). To clarify biochemical mechanisms responsible for this age specific paradox, we subjected 7-day postnatal rats to unilateral common carotid artery ligation followed by the hypoxia produced by the inhalation of 8% oxygen for 2hr (Rice et al, 1981). Experimental animals received 0.1 ml. 50% glucose sc 15 min prior to onset of hypoxia, which increased blood glucose to 350 mg/dl for 2 hr. Glucose in the cerebral hemisphere ipsilateral to the carotid occlusion was exhausted by 20 min of H-I in control (saline injected) rats but not until 2 hr in glucosetreated animals. Brain lactate and puruvate increased to a greater extent in the glucose-treated animals but only at 20 and 60 min, such that L/P ratios were comparable at 2 hr. Declines in ATP and P-creatine occurred earlier in control animals, but by 2 hr low levels were seen in both groups. Total adenine nucleotides also were depleted to the same degree. The findings indicate that despite an early protective influence of glucose on brain glycolytic intermediates & high energy reserves during cerebral H-I, the effect is short lived even with continuing hyperglycemia. Limited glucose entry into the immature brain at any blood glucose level retards anaerobic metabolism during H-I; which, in turn, leads to a disruption of the energy state of the tissue and ultimate brain damage. (NIH #HD-15738).

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