2. Endocrines and Populations 253 



drate metabolism in adrenalectomized rats (Dorfman, 1949; Ingle, 1950). 

 This response is a reflection of the ability of adrenal corticoids to stimulate 

 gluconeogenesis. Glycogen in the liver can be measured chemically (Marto- 

 rano, 1957) or can be visualized histochemically by the appropriate proce- 

 dures (Dempsey, 1948; Lillie, 1954). Liver glycogen presumably falls as a 

 result of exhaustion of the animal's ability to adapt (Frank, 1953) . Exactly 

 what becomes exhausted under these circumstances is problematical, but it 

 apparently is not the ability of the adrenal cortex to secrete steroids (Rosen- 

 feld, 1958) . Nevertheless, it is true that blood glucose and liver glycogen 

 eventually fall to extremely low levels following intense and prolonged 

 stimulation by alarming stimuli. This result may follow prolonged stimula- 

 tion of the sympatho-adrenal system. Exhaustion of glycogen, consequently 

 of glucose reserves, has been observed in natural populations of snowshoe 

 hares (Green and Larson, 1938; Green et al, 1939) and voles (Frank, 1953) 

 during episodes of mass mortality and may possibly be explained on the 

 basis of exhaustion of the adaptive reserves. 



A word of caution should be inserted on the use of liver glycogen as an 

 indicator or activity of the carbohydrate-active corticoids. Under carefully 

 controlled conditions in the laboratory such measurements are very useful, 

 but they do require rigid controls and precise, highly standardized proce- 

 dures. Martorano (1957) has studied the variables having important effects 

 on liver glycogen. The amount of time between killing and enzymatic 

 immobilization, the manner of killing, and a variety of other factors can 

 alter glycogen levels. Glycogen and glucose levels in the liver decline rapidly 

 after death. There also is a daily cycle in the levels of liver glycogen which 

 is associated with feeding and activity (Martorano, 1957). Therefore, re- 

 ported liver glycogen levels must be critically examined in relation to the 

 procedures used and their reliability. 



n. Changes in the digestive organs and gastrointestinal tract. Alarming 

 stimuli, ACTH, or cortisone produce a marked loss of the acidophilic 

 zymogen granules and basophilic cytoplasmic pentose nucleic acids from 

 the acinar cells of the pancreas and serous salivary gland cells (Ehrich and 

 Seifter, 1948; Selye, 1950). The pituitary adrenocortical system also pro- 

 foundly affects the function of the mucosa of the stomach and intestinal 

 tract (Baker and Abrams, 1954; Baker and Bridgman, 1954; Gray and 

 Ramsey, 1957). The adrenocortical hormone apparently stimulates the 

 secretion of pepsinogen by gastric zymogenic cells (Gray and Ramsey, 

 1957; Mason, 1959), which is reflected morphologically by a loss of the 

 intracellular pepsinogen granules and increased cytoplasmic basophilia 

 (Baker and Bridgman, 1954). Additional changes may not be noted histo- 

 logically in the mucosal cells of the intestine (Baker and Bridgman, 1954). 



