226 /. /. Christian 



reserves due to exhaustion of the supplies of epinephrine. Such a mecha- 

 nism, albeit conjectural, may provide a better explanation for the immedi- 

 ate and precipitate cause, the proximate cause, of "shock disease" than the 

 previously postulated pituitary- adrenocortical exhaustion (Christian, 

 1950b) , although adrenocortical hyperactivity probably plays an additive 

 or even synergistic role in the cause of the immediate mortality in "shock 

 disease." These conjectures are not meant to relegate the pituitary-adreno- 

 cortical-gonadal system to a secondary role in the more prolonged and 

 chronic effects of increased population density or in the control of popula- 

 tion growth, as we shall see later. However, the available experimental 

 evidence places the sympathico-adrenal medullary system in the forefront 

 of the mechanisms w^hich respond acutely and which need investigation in 

 relation to "shock disease" and the sudden and mass mortality associated 

 therewith, as well as in relation to those sudden deaths, resembling hypo- 

 glycemic shock, which occur on first placing strange mammals together. 



The development of techniques to measure the secretion of the catechol 

 amines has led to a number of investigations on the secretion of epinephrine 

 and norepinephrine in response to a variety of stimuli. One can almost pre- 

 dict which of these two amines will be secreted in response to a particular 

 stimulus by knowing which has the greater effect on blood sugar or on blood 

 pressure. Norepinephrine appears to be released preferentially by the adre- 

 nal medulla during rest (Gaddum and Holzbauer, 1957). The plasma 

 concentration of norepinephrine rises sharply with acute muscular work, 

 but the response of epinephrine varies from no change to a marked rise, 

 depending on the individual (Gray and Beetham, 1957). Both return to 

 normal levels within 15 to 30 minutes after cessation of work. Hypoglyce- 

 mia is followed by a marked and sharp rise in the medullary secretion of 

 epinephrine with a much less marked rise in norepinephrine (Gaddum and 

 Holzbauer, 1957; Goldfien ct al., 1958). Infusion of glucose promptly re- 

 turns their secretion to normal levels. Repeated production of hypoglyce- 

 mia with insulin eventually leads to a decline in the secretion of epinephrine, 

 evidently due to medullary exhaustion (Elmadjian ct al., 1958). Hypoten- 

 sion produces a marked rise in the secretion of norepinephrine, but little or 

 no rise in epinephrine (Elmadjian et al., 1958). Surgical shock or a change 

 in position from recumbent to standing leads to a sharp rise in the secretion 

 of norepinephrine with or without a rise in epinephrine. (Elmadjian et al., 

 1958). Tense, anticipatory but passive emotional situations produce a 

 marked rise in the secretion of epinephrine, norepinephrine being secreted 

 in normal amounts, but active, aggressive emotional situations are related 

 to a rise in norepinephrine (Elmadjian et al., 1958) . If the emotional display 

 is intense enough, both epinephrine and norepinephrine are elevated. It is 

 of particular interest that in adrenalectomized patients the secretion levels 

 of norepinephrine and their diurnal variations are completely normal. 



