GENERAL METABOLISM— HORVATH and SPURR 17 



ELF.CTROLYTES 



Sodium. S\v:m cl al..^" I'lfuiino-." McMillan ct al.'- and Dcterlino- cl a/.'-' have 

 rc'iJorU'd that the concentration of serum sodium docs not change appreciahly dur- 

 ing hypothermia. Da Costa ct al:*^ also ohserved no change in cyanotic dogs suh- 

 jected to hypothermia. Oshorn'"' found that, in general, serum sodium decreased 

 in concentration though no values were reported. 



Potassium. The changes which occur in the plasma or serum concentrations of 

 potassium during hypothermia are less clear-cut than for sodium. Fleming,*^ Deter- 

 ling et al.^'- and Da Costa et a/.^' found no significant change in plasma potassium 

 at low hody temperatures. McMillan ct al.^'- also found little change in plasma potas- 

 sium either for dogs which were respiring spontaneously during the hypothermia 

 or for dogs in which artificial respiration was maintained at 24 cycles/min. through- 

 out the cooling procedure. The latter group of animals demonstrated an average 

 decrease in potassium to ahout 85 per cent of the control value (3.5 to 3.0 mEq/L.). 

 This rate of ventilation, at low body temperatures, would represent a hyperventila- 

 tion of the animals. There was a progressive washout of carbon dioxide to as low as 

 12 vols, per cent at rectal temperatures of 22° C. However, Swan et al.*^ found that 

 hyperventilation alone (50-60 cycles/min.) produced a decrease in potassium to 

 about 70 per cent of control. 



Bigelow, Lindsay and Greenwood^^ found a consistent increase in serum potas- 

 sium concentration in dogs and Elliot and Crismon*^ reported that the cooled rat 

 demonstrated a rise in serum potassium from a mean value of 3.55 ±0.64 to 5.28 

 ±0.70 niEq/L. at rectal temperatures of 25° C. Since potassium did not increase 

 to a toxic level, the question arose regarding altered sensitivity of response in hypo- 

 thermic animals. The latter authors found that injections of potassium salts which 

 were well tolerated by the normothermic rats resulted in fatal potassium poisoning 

 when injected into hypothermic rats. If the hypothermic animals were given oral 

 glucose or injection of calcium chloride or ouabain previous to the potassium injec- 

 tions, protection against the lethal efTects of the^ latter was obtained. Fenn*^ had 

 found previously that the storage of glycogen in the liver involves an increase in 

 both hepatic water and potassium. When release of the previously stored carbo- 

 hydrate occurs there is a simultaneous release of water and potassium. Fuhrman and 

 Crismon"- had reported a sharp lowering of liver glycogen in cooled rats and 

 Samaras'^ found that an effective method of rendering the dog's liver glvcogen- 

 free was the induction of shivering by exposure to cold. Combining these results, 

 Elliot and Crismon^' attributed the rise in serum potassium observed in their experi- 

 ments, at least in part, to the release of potassium by the breakdown of liver glyco- 

 gen, and the protection afforded by oral glucose to the maintenance of a high liver 

 glycogen. Furthermore, muscular activity is known to deplete muscle of potassium*^ 

 and to bring about an increase in plasma potassium.^" Consequently, part of the 

 increase in potassium seen in hypothermia may be due to the increased muscular 

 activity of shivering. 



Swan ct al.*^ found a consistent decrease in serum potassium in hyperventilated 

 dogs during hypothermia. They reasoned that there was a shift of potassium to the 

 intracellular phase since the loss could not be accounted for in the urine. During oc- 



