280 PHYSIOLOGY OF INDUCED HYPOTHERMIA 



Temperature gradients. Although little mention was made of the existence of 

 temperature gradients in the deep parts of the body during hypothermia, this field 

 needs more careful study. The rectal and colonic temperature, although the stand- 

 ard reference for most work, have been found by us to be as much as \2° C. lower 

 than the central aortic and esophageal temperatures during rapid surface cooling 

 after vagotomy, and 4° C. higher or lower than esophageal temperatures in man 

 during surface cooling. If hypothermia is to be a study of function versus tem- 

 perature it is manifest that a correct estimation of central body temperature is 

 needed. The reviewer would conclude that best access to this temperature is in the 

 lower esophagus adjacent to the heart. In our experience the esophageal tempera- 

 ture was found to correlate much better than rectal temperature with oxygen 

 consumption. 



Temperature regulation. The temperature regulation center appears to have 

 been accurately localized in dogs to the posterior hypothalamic gray matter. When 

 this area or its connection to the mid brain was destroyed, poikilothermic animals 

 were obtained who showed normal basal metabolic rates at Z7° . It was noted that 

 destruction of either of two endocrine centers, the anterior hypothalamus and the 

 pituitary, lowers the basal metabolic rate, but transection of the pituitary stalk 

 joining them does not. Recent evidence suggests that the dog retains some tem- 

 perature regulation even at 24° C. during prolonged hypothermia. 



Nervous system. A considerable part of the interest in hypothermia is in pro- 

 tecting the central nervous system from ischemic damage, yet relatively little re- 

 ported work defines the exact parameters of safe time, or of damage at various 

 intervals of time. If one may assume that the higher centers are most easily 

 damaged, it would seem that post-hypothermia cerebral damage should not be 

 judged by ataxia or coma, but by the finer psychometric determinations available 

 today both for animals and man. Psychologists and psychiatrists should find in- 

 teresting material in post-hypothermic patients which to date have largely been 

 judged by relatively crude tests. 



There is considerable disagreement about the damage to nervous tissue that may 

 be produced by low temperatures. One group pumped cold blood into one carotid 

 artery in the dog and found damage when the brain temperature fell below 12° C. 

 on the colder side. However, the pressure used to perfuse was not reported, and 

 either excess pressure, the extremely low pCOo in the perfusate, the high pH, cur- 

 rents resulting from local extreme cold, or temperature gradients, might be im- 

 plicated. Other workers have cooled monkeys and dogs to lower temperatures 

 without observing post-hypothermia brain damage. Peripheral nerve palsies can 

 occur from prolonged ice water immersion, without frostbite. The recovery of 

 electrical activity of the cortex after 1 minute of ischemia is reported to be most 

 rapid at about 30° C. ; however, to assume that this is therefore the safest tempera- 

 ture for clinical hypothermia with blood flow occlusion is unjustified, since the 

 slower recovery at lower temperatures may not indicate increased damage. 



A new approach to the analysis of brain activity with low temperatures was 

 described in connection with awake poikilothermic dogs. These unanesthetized ani- 

 mals could be observed during cooling, and were found to function surprisingly 

 well, showing emotional and physical responses only slightly depressed, and eating 



