14 



PHYSIOLOGY OF INDUCED HYPOTHERMIA 



12 3 4 



12 



16 20 



TIME IN HOURS 



Fig. 4. — Rectal, mean skin, mean body temperatures and heat content of a dog that was stable 

 at a rectal temperature between 23.5-24.0° C. for 34.1 hours. At the end of this time ventricular 

 fibrillation occurred and death ensued. 



liver glycogen. The blood glucose then remained elevated throughout the remainder 

 of the hypothermia. Furthermore, in starved animals or slowly-cooled fed animals 

 the blood glucose w^as maintained or fell during cooling. Slow cooling for prolonged 

 periods has been demonstrated by others to result in hypoglycemia.""- ^'^ The evi- 

 dence therefore seems to indicate the necessity of differentiating between shivering 

 and non-shivering animals during the initial stages of cooling, and between chronic 

 and acute hypothermia. Also, the carbohydrate stores of the animal nuist be con- 

 sidered. In the presence of shivering, provided the animal's source of carbohydrate 

 is adequate, blood glucose increases. In acute hypothermia further reduction of body 

 temperature results in cessation of shivering and a consequent reduction in meta- 

 bolic rate and utilization of carbohydrate. Thus, the early hyperglycemia is main- 

 tained.^- If the reduction in body temperature is prolonged, shivering persists with 

 a consequent exhaustion of liver and muscle glycogen and a resulting hypoglvcemia. 

 In the absence of shivering during cooling, the blood glucose level mav be maintained 

 or decreased.-^- 



Necrosis of depot fat may be caused by exposure to cold. I locksinger '"and llaxt- 

 hausen''- have reported cases of subcutaneous fat necrosis in children following 

 exposure to low temperatures. 1'his tendency to develop fat necrosis may be de- 

 pendent upon the chenn'cal composition of the fat ])resc'nt. The melting ]X)int of sub- 

 cutaneous fat of children is nuicli hii'lier and has a lower iodine nuniln'r than that 



