132 The Chemistry of the Injured Cell 



Although release of adrenaline from the suprarenal medulla is 

 a vital feature of the immediate response to injury, its action on 

 carbohydrate metabolism in this situation appears to be partly in- 

 direct. Thus in the absence of the pituitary gland the characteristic 

 adrenaline effects on blood sugar are greatly diminished. In ad- 

 dition, the action of adrenaline on carbohydrate metabolism may 

 be largely reproduced by injections of adrenocorticotropic hor- 

 mone (ACTH) from the pituitary. These observations indicate 

 that some of the actions of adrenaline in the immediate reaction to 

 injury are due to increased secretion of ACTH which in turn 

 causes increased secretion of cortical hormones from the suprarenal. 

 In fact adrenaline causes increased adrenocortical secretion (Vogt, 

 1943) and depletes the ascorbic acid and cholesterol content of the 

 adrenal cortex (Long and Fry, 1945) , a sign of increased secretion. 

 ACTH has similar effects. There is some evidence that the altera- 

 tions in carbohydrate metabolism depend on the integrity of the 

 hypothalamus (De Groot and Harris, 1950) and it is known that 

 secretion of ACTH may be induced directly by nervous stimuli 

 (Vogt, 1952) . Thus it may be that adrenalin stimulates the pituitary 

 by way of the hypothalamus. 



Injury Adrenal Adrenaline Hypothalamus 



medulla 



Ant. Pituitary .ACTH .Adrenocortical hormones 



Apart from the changes in blood glucose, etc., already described, 

 there are at least five common sequelae to injury, indications of 

 increased adrenocortical function, all of which may be reproduced 

 by injection of ACTH and none of which occur in the absence of 

 the adrenal glands. They are a manifold increase in the excretion 

 of steroids derived from the adrenal cortex (Venning et. al., 1944), 

 enlargement of and a decreased level of ascorbic acid and choles- 

 terol in the adrenal cortex (Tefferman et al., 1943) , shrinkage of 

 lymphoid tissue in the body and a decrease in the level of circulating 

 eosinophil leucocytes and lymphocytes (Selye, 1946) . 



The second stage in the metabolic reaction to injury is the phase 

 of shock. Shock itself will be considered later. The chief metabolic 

 features of this period (whose relationship to the circulatory 

 changes of shock are obscure) are an increased level of blood amino 



