FREE 17-HYDROXYCORTICOIDS— BERNHARD 181 



in the unstressed individual, both human and dog, and we, too, so far have been 

 unable to study the effect of hypothermia in the unstressed individual. 



Dr. Hume was studying an animal essentially maximally stressed, and Dr. Bern- 

 hard's chart showed that in his experimental animals after the placement of the 

 cannulas, ACTH failed to produce any considerable additional rise in the corticoid 

 output, so when hypothermia was superimposed the animal being studied was in an 

 already stressed state. For that reason it is difficult to estimate the effect of hypo- 

 thermia on the corticoid output when it is already high. 



During a state of hypothermia it is not surprising that the cellular function is 

 apparently markedly depressed as is the cellular function of all the tissues of the 

 body when the cells are quite cold. So during the period of hypothermia this de- 

 pression of corticoid output is not surprising, but the response afterwards appears 

 to us to be the crux. 



We would like to be able to study the effect of hypothermia on an unstressed 

 animal. The critical consideration here, interestingly enough, is anesthesia. In Dr. 

 Bernhard's study the anesthetic agent used in the clinical series was apparently 

 always ether. We have been interested in the cortical response to different types of 

 anesthesia, and I would like to show you one slide in that regard. These are warm 

 patients. 



Figure 1 shows the corticoid response to one hour of anesthesia with pentothal 

 alone (or with cyclopropane) and with pentothal-ether. The corticoid response 

 averages an increase of 1 1 over the control value in six patients who had one hour 

 of ether anesthesia. On the other hand, pentothal or cyclopropane anesthesia in 14 

 patients appears to cause little or no response in corticoid output. For this reason 

 we plan now to proceed with the obvious step of inducing hypothermia with the 

 use of this anesthetic agent to see if we can study the response in the nonstressed 

 human. 



Figure 2 merely shows the possibilities of response. It would appear from Dr. 

 Bernhard's work that hypothermia delays the corticoid response to operation. We 

 show here the initial rise with anesthesia. Possibly with the proper anesthesia one 

 could obtain a straight, level line. One must then measure the immediate postopera- 

 tive response in the patient who has been under hypothermia. On the basis of pres- 

 ent evidence. Dr. Bernhard suggests that it falls in a mid-position, i.e., hypothermia 

 has not completely suppressed the adrenocortical response to surgery, but it has 

 both delayed and diminished it. It would be interesting to see if in the unstressed 

 animal hypothermia can suppress the cortico-corticoid response to trauma. 



