2. Endocrines and Populations 257 



be apparent now that most of these same stimuH also increase the secretion 

 of adrenocortical steroids. However, commonly accepted truisms still do 

 not constitute experimental evidence and proof of such conclusions, but 

 several experiments have shown that host resistance is decreased by ex- 

 posing the animals to stimuli which are known to increase adrenocortical 

 activity. When mice are exposed to 4° C. for a period of time, Coxsackie 

 infections become much more pathogenic, spreading especially to the heart 

 and liver in adult mice (Boring et al., 1956) . Duninished resistance of mice 

 to trichinosis and to tuberculosis has been demonstrated by procedures 

 which also produce increased pituitary-adrenocortical activity and depress 

 inflammation and granulation (Christian and Williamson, 1958; Tobach 

 and Block, 1956; Davis and Read, 1958) . Some aspects of these studies will 

 be considered in more detail later. 



e. Reproduction. Suppression of reproduction is a very important aspect 

 of the endocrine adaptive responses (Selye, 1939, 1950). The decrease in 

 reproductive function is in many ways a more sensitive measure of the 

 existence of altered physiologic functions in response to adversity than the 

 increase in adrenocortical activity and some of its sequelae (Christian, 

 1955a, b, 1956, 1959b, c) . The bulk of the experimental evidence indicates 

 that, like growth hormone, the secretion of pituitary gonadotropins is sup- 

 pressed in response to alarmmg stimuli which evoke an increased secretion 

 of ACTH (Selye, 1939, 1950; Christian, 1956, 1959b, c). It is another 

 indication that the immediate restoration of the normal internal environ- 

 ment takes precedence over functions which are less important to the im- 

 mediate siu-vival of the individual. Cold, heat, disease, trauma, severe 

 emotional stress, and other stimuli will depress normal reproductive func- 

 tions (Marrian and Parkes, 1929; Selye, 1939; Bohanan, 1939; Poindexter, 

 1949; Denison and Zarrow, 1955; Barnett and Manly, 1956; Christian and 

 LeMunyan, 1958; Christian, 1959b). The suppression of gonadotropin 

 secretion is evidently the primary cause of the inhibition of reproductive 

 function (Mulinos et al, 1939, Selye, 1950; Srebnik et al, 1958), although 

 there may be direct effects of increased adrenocortical activity and altered 

 thyroid function, as mentioned earlier (Brynes and Shipley, 1950; Baker 

 et al, 1950; Smith, 1951; Brimblecombe et al, 1954). The secretion of 

 gonadotropins seems to be regulated principally by the hypothalamus 

 (Anderson and Haymaker, 1948a, b; Markee et al, 1952; Everett and 

 Sawyer, 1953; Hammond, 1954; Critchlow and Sawyer, 1955; Nalbandov 

 et al, 1955; Laqueur et al, 1955; Fortier, 1957; Greer, 1957; D'Angelo and 

 Traum, 1958 Everett, 1959) , although there is evidence that the secretion 

 of luteotropin by the pituitary may be independent of the hypothalamus 

 (Everett, 1956). The hypothalamic centers involved in the regulation of 

 the secretion of the gonadotropins apparently are distinct from those 



