136 ELECTROLYTES IN BIOLOGICAL SYSTEMS 



Green and Parpart found that lAA promotes K loss in rabbit red cells in the 

 absence of glucose (32). 



NaF also inhibits both glycolysis and the net accumulation of K and ex- 

 trusion of Na (12, 38, 58). This compound probably blocks glycolysis by in- 

 hibiting enolase though in high concentrations it will inhibit many enzymes 

 requiring Mg for activity (52). When human red cells are suspended in .03 

 m/1. NaF, the fluoride ion penetrates the cell very rapidly, and produces net 

 K loss without an equal Na gain (18, 120). This difference in effect on Na and 

 K does not occur in .01 m/1. NaF (58). Studies of the effect of NaF on K fluxes 

 with K^- indicate that effect of the inhibitor varies with the concentration 

 used (21). At a NaF concentration of .005 m/1. K influx is reduced and outflux 

 little affected. When the concentration is .02-.025 m/1. K influx is decreased 

 but outflux is accelerated (104). Eckel has made a more extensive study of the 

 effects of higher concentrations of NaF on K fluxes measured with tracer 

 (19, 20). He found that .025 m/1. NaF increased both net K loss and the K 

 exchange rate. He interprets his findings to indicate that exposure to .025 

 m/1. NaF gives rise to a rapidly exchanging compartment of cell K. This 

 compartment begins to appear about i3^^ hours after exposure to NaF and 

 comprises 65 to 95 % of the cell K at the end of 4 hours exposure. This com- 

 partment exchanges K about 200 times faster than normal cell K. .120 m/1. 

 NaF simulated the effect of .005 m/1. NaF. Pyruvate (.003-.010 m/1.) restored to 

 normal the reduced K influx caused by .005 m/1. NaF, and inhibited the de- 

 velopment of a rapidly exchanging K compartment in .025 m/1. NaF (21). NaF 

 (.005 m/1.) also inhibits Na outflux (35). As in the case of lAA, NaF accelerated 

 net K loss from rabbit red cells even in the absence of glucose (32). NaF pro- 

 duces K loss in the red cells of rabbit and rat, but not in those of horse and 

 pig which glycolyze only very slowly (18). In summary, the effects of lAA 

 and NaF on cation transport in human red cells are compatible with the idea 

 that the compounds act in two ways: /) by inhibiting glycolysis and thus 

 glycolysis-linked reactions responsible for K influx and Na outflux, and 2) 

 by increasing the rate of diffusion of K and Na across the cell membrane. The 

 latter effect is particularly evident at higher concentrations of NaF. 



A variety of metabolic poisons which do not, in the concentrations used, 

 inhibit glycolysis, also fail to affect the net re-accumulation of K and extrusion 

 of Na by previously cold stored human red cells (58). These include NaCN, 

 2-4 dinitrophenol, NaNs , and CO, all of which actually increased glycolysis. 

 Methylene blue, which markedly stimulates the respiration of red cells, sulfanil- 

 amide, which inhibits carbonic anhydrase, and malonate were also without 

 effect on net cation transport. 



Hydrogen ions can also be looked upon as a metabolic inhibitor in human 

 red cells since they inhibit glycolysis and promote the breakdown of cell 



