Shock and Related Phenomena 133 



nitrogen due either to decreased deamination in the liver (possibly 

 due to hepatic anoxia) or to loss of amino acids from muscle (Engel 

 et al., 1944) and a general blockage of carbohydrate breakdown 

 (Threlfall and Stoner, 1954) . This last disturbance is manifest as a 

 reduced output of energy leading to lowered body temperature and 

 decreased oxygen consumption and as a general depletion of bodily 

 carbohydrate and breakdown of labile phosphate esters especially 

 creatine phosphate, possibly in response to lack of oxidisable sub- 

 strate (Ord and Stocken, 1955) . It is thought that this disturbance 

 of carbohydrate metabolism, too, may be due partly to increased 

 secretion of adrenocortical hormones causing reduced glucose utili- 

 sation (Engel, 1951) . 



The chief metabolic feature of the recovery phase of injury, 

 seen after twenty-four hours or so have elapsed, is the increased 

 excretion of urea nitrogen, sulphur and phosphorus (Cuthbertson, 

 1954) . Since nitrogen loss varies directly with the protein level of 

 the diet the source of these substances appears to be the more labile 

 and rapidly metabolised proteins of the body particularly the liver 

 and skeletal muscles. There seems to be in fact an abnormally rapid 

 breakdown of such protein in this phase of injury and the abnormal 

 catabolism can be partially prevented by administration of carbo- 

 hydrates, suggesting that increased glyconeogenesis (formation of 

 glycogen from protein) is responsible. The rapid breakdown of 

 protein and consequent formation of glycogen can be reproduced 

 by injection of ACTH and adrenocortical hormones and, as in in- 

 jury, can be prevented by administration of carbohydrate (Long 

 et al., 1940) . Moreover, loss of nitrogen after experimental injury 

 does not occur if the animal has been previously adrenalectomised. 

 Thus once again it would appear that the changes observed are due 

 to stimulation of the adrenal cortex. However, it has been shown 

 that injury will in fact cause increased nitrogen excretion in adrena- 

 lectomised animals provided that a small maintenance dose of 

 adrenocortical extract is given. It seems, therefore, that although 

 injury cannot cause excessive protein breakdown in the absence of 

 circulating cortical hormones, this metabolic reaction is not due 

 directly to stimulation of the adrenal cortex (Ingle et al., 1947; 

 Engel, 1951; Campbell et al., 1953) . In what fashion injury and 



