Prolonged anoxic survival due to anoxia pre-exposure: brain ATP, lactate, and pyruvate

Abstract

Rats subjected to a brief anoxia can survive go sec in a second anoxia, compared to a 60-sec survival time of control animals. Slower disappearance of ATP concentration in the brain during the second exposure indicates this longer survival is due to an altered cerebral energy metabolism. Initial cerebral ATP concentration is no higher in pre-exposed animals than in controls. When glycolysis is inhibited by iodoacetate before testing in anoxia, the advantage of pre-exposure disappears, suggesting the longer survival may be due to increased anacrobic glycolysis. Lactate accumulates faster during anoxia in the brains of pre-exposed animals than in controls, suggesting that increased anaerobic glycolysis is the cause of the prolonged survival. This effect is not due to increased cerebral glucose concentration. A possible reason for this increased glycolysis, and thus the prolonged survival, could be an increase of a compound, such as pyruvate, capable of oxidizing NADH. The initial pyruvate is higher in pre-exposed animals than in controls and injection of pyruvate increases the survival time slightly.