Pyruvate labeled with carbon-14 was administered intraperitoneally to newborn rats which were subsequently subjected to periods of aerobiosis or anaerobiosis. Expired air was analyzed for carbon dioxide, and blood, liver and carcass were analyzed for pyruvate, lactate, glycogen and total lipids. Small quantities of CO2 were produced anaerobically but this was not derived from the direct decarboxylation of pyruvate. Anaerobiosis resulted in a five-fold increase in blood lactate. The liver glycogen content of 10–24-hr-old rats treated anaerobically was only 10% of that of those kept in oxygen. The premature and newborn rats were apparently unable to mobilize glycogen in response to anoxia. The amounts of liver or carcass lipids were not significantly different after aerobic or anaerobic conditions. Lipogenesis occurred anaerobically at a rate not greatly different from that observed in aerobic conditions. In contrast, the data suggest that the utilization of lipids is reduced by anaerobiosis. No gross changes were found that could entirely explain the ability of neonates to survive prolonged oxygen deprivation but part, at least, of the energy for survival was provided by accelerated glycolysis.
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