METABOLISM IN CHANGED CEREBRAL ACTIVITY 49 



glucose was present in the perfusate. However, continuing 

 perfusion in the presence of glucose did not prevent an overall 

 decrease in the total phospholipid phosphorus and an impairment 

 in the ability of the brain to oxidize glucose. Interestingly, these 

 defects could be prevented if small amounts of cytidine and uridine 

 were added to the perfusion fluid (Geiger and Yamasaki, 1956). 



The mechanism by which these latter effects are mediated is not 

 known. It is also difficult to attempt correlations of changes in the 

 perfused brain with changes in the hypoglycaemic animal. Never- 

 theless the evidence shows that hypoglycaemia in addition to 

 causing immediate changes in energy producing systems can also 

 lead to extensive and probably irreversible catabolism of phosphates 

 which are likely to be part of structural components in the brain. 

 In this connexion it perhaps is of interest to note that lesions 

 developing in various areas of the brain following severe hypo- 

 glycaemia almost invariably include a loss of Nissl bodies (Meyer, 

 1958) which, it is suggested, are likely to form part of the micro- 

 somal fraction (cf. Einarson, 1957). 



Hypoxia^ Hypothertnia and Related Influences 



In man, a reduction in arterial oxygen tension to 24% leads 

 to loss of consciousness (Lennox et al., 1935) though the oxygen 

 uptake of the brain appears to be normal when the inspired air 

 contains 10% oxygen (Kety and Schmidt, 1948). As is well known, 

 brief periods of partial or complete hypoxia can lead to symptoms 

 such as loss of memory and occasionally convulsions, associated 

 with histologically demonstrable degeneration in selected cells and 

 areas of the brain (see Meyer, 1958). 



As may be expected, change in the cerebral oxygen supply is 

 accompanied by changes in the quantities of energy-rich phos- 

 phates, the extent of the change being related to the degree of 

 hypoxia. In animals breathing gas mixtures via a tracheal tube a 

 gradual reduction of the percentage of oxygen in the inspired air 

 did not affect levels of cerebral phosphocreatine until the arterial 

 oxygen saturation was about 20% (Gurdjian et al, 1944; Gurdjian 

 et al.^ 1949). Cerebral lactic acid began to increase when the 

 oxygen in the inspired air reached 11-13%, corresponding to a 

 level of saturation of 55-65% in arterial blood and 28-43% in the 

 sagittal sinus. Further reduction to 7% oxygen in the inspired air 

 induced phosphocreatine breakdown, at which the saturation was 



