PITUITARY AND ADRENALS— HUM K, KGDAHL and NF.LSON 



171 



conditions and the dog was allowed to recover. The animal was then exposed to 

 cold three or four days later, when his adrenal corticosteroid secretion had reached 

 hasal levels. Three such (l()j;s were anesthetized with nenihutal and rendered h\po- 

 therniic in an ice water hath, without the addition of any trauma. 

 Results. The results may ])e summarized as follows: 



1. Pituitary ACTH secretion in the traumatized animal decreases markedly dur- 

 ing hypothermia, and resumes high levels again on rewarming^- " (fig. 1). 



2. Adrenal 17-hydroxycorticoid production in the traumatized animal is de- 

 creased to very low levels during hypothermia and retm-ns rapidly to normal on 

 rewarming.^' ^ 



3. Corticoid output is decreased in hypothermia e\en if the systemic hlood pres- 

 sure is maintained at near normal levels.-' " 



4. The adrenal is unresponsive to large doses of ACTH while the animal is 

 hypothermic, and the response rapidly returns on rewarming.-' " 



5. Cold appears to act directly on adrenal enzyme systems. When local cold is 

 applied to the adrenal and the animal remains normothermic the adrenal corti- 

 costeroid secretion is sharply reduced.-' ^ 



Temp 

 Cent 



37 5 37.0 370 



26 210 



32 37 5 



AVB 17-OH Corticosteroids 

 Plasma ACTH Milliunits/lOO cc. 



5 « 



-31 



- 2 



- 1 



CONTROL PERIOD 



Fig. 1. — The blood ACTH levels and adrenal vein blood 17-hydroxycorticosteroid output in 

 a dog traumatized under ether anesthesia and then subjected to hypothermia. It may be seen 

 that there is a marked depression of corticosteroid secretion during hypothermia, with an in- 

 crease again after rewarming. Blood ACTH, which is at a measurable level before the induction 

 of hypothermia, becomes too low to measure during hypothermia. On rewarming, ACTH is 

 again present in easily detectable amounts. 



