174 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



very greatly reduced. It is difficult, therefore, to get an accurate idea of adrenal 

 steroid production by measuring peripheral levels of corticoids in hypothermia. 



The second point is that the dog appears uniquely able to withstand severe cold. 

 Cold at —10° C. does not increase corticoid production, and the adrenalectomized 

 dog can withstand this temperature without ill effect. Apparently even the induc- 

 tion of hypothermia under anesthesia is not a stimulus to the hypothalamic- 

 pituitary-adrenal system in this species. 



Dr. J. R. Pappenhcimer: Is chemical therapy a good or bad thing? Is there 

 any difference in the survival of animals if they are given supplementary doses of 

 drugs ? 



Dr. Moore: Thank you, Dr. Pappenheimer. 



In answer to your question, we may anticipate a bit. In the next talk, Dr. Bern- 

 hard will show an anesthesia chart which is one item in a fairly broad study that we 

 are now doing on the effect of anesthetic agents on the stress mechanism, or what- 

 ever you want to call it, in man. I also expect that, in the discussion to follow, Dr. 

 Swan will refer to his studies on the effect of drugs in hypothermic subjects. Some 

 of our work has been along the same lines. During the past three years we have 

 found that pentothal, nitrous oxide, curare, cyclopropane — spinal and local — are all 

 of interest in that they provide a very mild or practically zero stimulus to adreno- 

 cortical secretion as measured in the peripheral blood. 



Cyclopropane is interesting since it does not stimulate the adrenocortical system, 

 but information we have obtained in collaboration with Dr. Aronow indicates that 

 it does stimulate the epinephrine-norepinephrine system, and it is a very strong 

 stimulant to anti-diuresis. So we are beginning to see dissociations in various types 

 of endocrine stimulation with different agents. "Stress" covers a multitude of 

 phenomena. Ether leads the list in causing a rise in the serum corticoids. 



As a patient recovers from a surgical operation which involves a big cross-sec- 

 tional tissue trauma, he will have a secondary rise in serum corticoids as he comes 

 out of the anesthetic agent. The obvious explanation has to do with pain. We can't 

 prove that that is the case. 



In the experiments planned by Dr. Swan it will be interesting to see what hap- 

 pens. If the animal is traumatized under hypothermia and then comes out of both 

 the hypothermia and the anesthesia, it would be my prediction he would tlien show 

 a peripheral rise in 17-hydroxysteroids. 



Two or three things can be said about the teleology of all this. First, if an animal 

 is incapable of summoning any endocrine response to trauma, the animal does very 

 poorly. Second, there are circumstances in which the endocrine response to trauma 

 appears to be massive, as evidenced either in terms of nitrogen-potassium changes, 

 or measurements of corticoids in blood or urine, and those patients seem to be very 

 sick as if something "overshot." Third, it seems that we are seeing a "middle 

 ground" in hypothermia which does not inhibit the adrenal to the point that the 

 patient or the animal responds like an addisonian, and \et produces a modified 

 response. It is probably a good thing that the adrenal activity is not completely 

 inhibited, but is somewhat restrained. 1 have been impressed by this in the ten or 

 twelve patients we have observed. Under hyi)otliermia, an amount of ojH'rative 

 trauma which the next day should produce a very sick-looking patient instead 

 produces a mild but normal posttraumatic reaction. 



