Abstract
To ascertain cerebral metabolic responses to hypoglycemia with superimposed hypoxia, newborn rats were given regular insulin (30 u/kg s.c.). Animals were observed for up to 2 hrs with no ill effects, inspite of blood glucose concentrations of 0.75 mM/1. When exposed to 100% N2 at 37°C, these animals survive only 1/10 as long as littermate controls with normal blood glucose levels (4.7 mM/1). Treatment of hypoglycemic rats with glucose (25 mM/kg s.c.) 30 min prior to N2 exposure prevented the anoxic vulnerability. Glycolytic intermediates & high-energy phosphate reserves (mM/kg w.w.) in brains of control (C) hypoglycemic (H) & hypoglycemic-glucose treated (H-G) animals breathing air were:
The cerebral metabolic rate (CMR) was not altered by hypoglycemia & averaged 2.32 mM∼P/kg/min. Following 2.5 min of N2 exposure, the cerebral energy stores ATP & P-Cr in hypoglycemic rats were lower by 24 & 51%, respectively, compared to normoglycenic animals subjected to the same degree of anoxia. Thus, reduced anoxic resistance of hypoglycemic neonates is not primarily a function of lower brain glycogen level* or altered CMR. Endogenous cerebral glucose stores combined with continued circulating glucose (cerebrovascular perfusion) appears critical for maintaining perinatal hypoxic survival.
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Vannucci, R., Vannucci, S. & Nelson, N. CEREBRAL METABOLIC EFFECTS OF NEONATAL HYPOGLYCEMIA AND ANOXIA. Pediatr Res 11, 523 (1977). https://doi.org/10.1203/00006450-197704000-00917
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DOI: https://doi.org/10.1203/00006450-197704000-00917