254 /. /. Christian 



3. Generalized Effects of Physiologic Adaptation 



a. Growth. Associated with acute adaptation there is usually a suppres- 

 sion of growth (Selye, 1950) . Selye (1950) has suggested that during actua- 

 tion of the pituitary-adrenocortical system there is a decreased production 

 of the other hormones of the adenohypophysis, including growth hormone. 

 However, injected corticoids or ACTH into intact animals also results in 

 suppression of growth and ACTH will inhibit growth produced by growth 

 hormone in h^Tpophysectomized rats (Jones, 1957). It was pointed out 

 earlier in this chapter that the adrenal carbohydrate-active corticoids in- 

 crease protein catabolism, prevent the gro^^iih of bone, lymphoid tissue, 

 skin, connective tissue with the production of collagen, and block mitoses 

 in general. Therefore the suppression of growth by alarming stimuli may 

 reflect decreased secretion of growth hormone as well as the direct suppre- 

 sive action of the carbohydrate-action corticoids on mitoses and therefore 

 growth and development. Diminished thyroid activity during periods of 

 actively increased adrenocortical activity may also play a role in this phe- 

 nomenon. Selye (1950) has pointed out that most of the observed changes 

 following an alarmmg stimulus serve to maintain life and that other, less 

 immediately important, functions are suppressed. 



b. Inflammation and granulation. The adrenocorticoids, cortisone, hydro- 

 cortisone, and to a lesser extent corticosterone, exert powerful anti- 

 inflammatory effects which stem from the suppression of growth of connec- 

 tive tissue, the depression of Ij'mphocyte activity, and interference with 

 the phagocj^tic process (Dougherty, 1953; Robinson and Smith, 1953; 

 Thomas, 1953), but in addition they prevent the mobilization of all of the 

 usual elements of an inflammatory response around the site of injury 

 (Taubenhaus and Amromin, 1950; Dougherty, 1953; Robinson and Smith, 

 1953; Gordon, 1955; Dougherty and Schneebeli, 1955). Androgens and 

 estrogens potentiate these anti-inflammatory responses. They decrease the 

 destruction of fibroblasts and the invasion of polymorphonuclear leuco- 

 cytes and macrophages. The appearance of epithelioid macrophages, giant 

 cells, and formation of new fibroblasts and macrophages are suppressed by 

 cortisone, either injected or implanted as pellets (Baker, 1954) . Dougherty 

 and Schneebeli (1955) explain the inhibition of the inflammatory response 

 around the site of injury in the following way: When there is cellular injury, 

 substances are released from the injured cells which trigger a series of re- 

 sponses which comprise inflammation (Menkin, 1955; Dougherty and 

 Schneebeli, 1955). Cortisone or hydrocortisone inhibit the inflammatory 

 response by protecting the surviving cells from the actions of the released 

 products of cellular injury. Growth hormone, deoxycorticosterone, and 

 aldosterone appear to exert a stimulating effect on inflarmnation and the 



