METABOLISM IN CHANGED CEREBRAL ACTIVITY 



51 



by the breakdown of phosphocreatine and adenosine triphosphate. 

 The source of this additional phosphate is not known. 



Hypothermia, which in itself is without any marked effect upon 

 the normal levels of energy-rich phosphates in the brain (Sav- 

 chenko, 1958) retards their breakdown in anoxia (Table 8). Thus 

 a drop of 11° is sufficient to extend the period of breakdown by 

 some 5-10 min. Such a retardation accords well with the known 

 increases in survival time of rats under anoxic conditions but at 



Table 8. — The Effects of Anoxia upon the Quantities of Adenosine 

 Triphosphate, Phosphocreatine and Inorganic Phosphate in Brain 



Data from Thorn et al. (1958) and Isselhard et al. (1959). 



Rabbits were rendered anoxic by administration of nitrogen via a 

 tracheal tube. The brain was frozen in liquid nitrogen before analysis. 



markedly reduced temperatures (Britton and Kline, 1945; 

 Himwich, 1951). 



Restoration of normal levels of phosphocreatine following 

 depletion in anoxia is rapid provided that the period of anoxia has 

 not been prolonged. In the rabbit, breathing nitrogen for 2-3 min 

 reduces the levels of phosphocreatine. Artificial respiration at this 

 period was sufficient to restore the levels to normal or above 

 within 2-2i min (Stone et al, 1941). However, anoxia induced by 

 breathing 4-2% oxygen for 15 min required a recovery period of up 

 to 1 hr before levels of inorganic phosphate, lactic acid and the 

 e.e.g. returned to normal, though levels of phosphocreatine were 

 resynthesized much sooner (Gurdjian et al., 1944). 



