PERINATAL BRAIN METABOLISM: EFFECTS OF ANOXIA AND ISCHEMIA

Abstract

Resistance to anoxia is characteristic of developing nervous tissue, and is most pronounced in the fetus. Whether this tolerance resides in differences in structural-functional maturity or in metabolic factors i.e. “resting” levels of cerebral energy reserves, rates of energy utilization, or glycolytic capacity is unresolved. Fetal rats at term, delivered by maternal decapitation and hysterotomy, survive in N₂, at 37°C (LD₈₅=50 min) twice as long as 1-day (1D) and 5 times as long as 7-day (7D) postnatal rats. Total energy reserves in quick-frozen forebrains [˜P=2(ATP)+ADP+P-creatine+2(glucose)+2.9 (glycogen)] of fetuses (27.0 mM/Kg) were 11% and 13% higher than in 1D and 7D rats, owing chiefly to differences in glycogen. Following decapitation, lactate accumulated in fetal and 1D brain in linear fashion up to 5 min (maximal glycolytic flux), but at a greater rate in fetuses (0.97 vs 0.69 mM/Kg/ min). In 7D rats maximal lactate production (1.94 mM/Kg/min) occurred from 1-2 min, following a lag. From the changes in preformed and potential cerebral energy stores during ischemia initial rates of energy consumption (metabolic rate) were obtained (Lowry et al, 1964). In fetal and 1D rats, energy consumption was linear for 5 min with slopes of 1.57 and 1.33 mM ˜;P/Kg/min, respectively. In 7D rats energy use was linear for only 2 min and about twice as fast (2.58). Thus, in postnatal (1D and 7D) rats anoxic survival and cerebral energy consumption were inversely related; no such correlation was observed for fetal animals. (Supported by NIH #NS-03346)

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