216 



PHYSIOLOGY OF INDUCED HYPOTHERMIA 



During cooling (immersion in water, light nembutal anesthesia), the concentra- 

 tion of Na-* does not change appreciably in either the blood or in the urine. On 

 rewarming, however, usually when body temperatures over 30° C. are reached, a 

 marked fall of the urinary concentration of sodium occurs (fig. 3). The disap- 

 pearance of sodium from the urine toward the end of rewarming seems to be inde- 

 pendent of the antidiuretic hormone and some facts indicate that it may be related 

 to the hyperglycemia and glucosuria encountered in hypothermia (And jus and 

 Morel, 1952). 



In order to study the effect of hypothermia on the reabsorption capacity of the 

 renal tubules, two different ways of eliciting maximal reabsorption activity were 

 used. Maximal tubular reabsorption of sodium and consequently its disappearance 

 from the urine can be induced in rats either (1) by injecting hypertonic glucose 

 intravenously, or (2) by eliminating the antidiuretic hormone from the circula- 

 tion (temporarily, as in water diuresis, or permanently, as in operative diabetes 

 insipidus). 



RAT c? 2209 



^/cHalL 



Fig. 3. Spontaneous fall of sodium concentration in the urine toward the end of rewarming 



of a rat cooled to 15° C. (Andjus and Morel, 1952). From above downward: (1) Radioac- 

 tivity of the urine. The peaks are inversely proportional to the actual concentration of radio- 

 sodium in the outflowing urine (cNa U). (2) Time (minutes). (3) The rectal temperature. 

 (4) Drops of urine. 



