POTASSIUM EXCHANGl' IX IM'.RFL'SKD MUSCLK— REXKIN 35 



In the "fast" cc)ni])ai-tnH'iU. which prcsuniahly represents tlie \vell-i)erfuse(l re- 

 mainder of the tissues, the limiting step in the transport chain for K'- is not clearly 

 indicated. The low temperature coefficient, Q,,, about 1.2, suggests that transcapillary 

 or interstitial diffusion may be the limiting process. Transport of IC across cell 

 membranes l)y chemical binding to a carrier molecule might be expected to have a 

 Qio of about 2 or 3, characteristic of a chemical process. However, similarity be- 

 tween clearances of Xa'-^ and K^- at 35° makes it possible that here too. blood flow 

 may be the limiting step. In this event, one of the other processes with a higher tem- 

 perature coefficient must become rate-limiting at 5° C. Consequently, all we can say 

 about cell membrane exchange of K"^ at low temperatures is that K' influx must take 

 place at a rate equal to or exceeding the iniiiinial exchange rate listed in table 1, 

 0.17 per cent tissue K^ per minute in the rapidly equilibrating compartment. And 

 since net loss of K^ is about 0.004 per cent per minute, the outflux must be just this 

 much greater than the influx. 



Initially we observed that whereas thin strips of mammalian skeletal muscle im- 

 mersed in a bath of Ringer's fluid lose K* rapidly in the cold, perfused mammalian 

 skeletal muscle does not. We now come to the question of why this difference should 

 exist. The answer is entirely unknown at present. The most obvious difference be- 

 tween the two preparations is the distance through which diffusion of oxygen, tissue 

 metabolites and potassium takes place between the fluid medium and the cells. The 

 intercapillary distance in the perfused hindleg muscles is of the order of 50 micra. 

 the maximum diffusion distance is thus 25 micra. The thickness of the rat diaphragm 

 is about 0.4 to 0.5 mm., or 400 to 500 micra, the maximum diffusion path l)eing 

 half this, 200 to 250 micra. However, 250 micra should be thin enough for adequate 

 diffusion of ( ), and CO,, at 37° C, according to Hill's equations,^ and at lower 

 temperatures, since metal)olic processes are slowed more than diffusion, conditions 

 should be even more favorable. Nor does it appear that the presence of plasma or 

 protein in the perfusion fluid is responsible for the difference, since Taylor*^ found 

 no K* loss in heart muscle perfused with protein-free media in the cold. Continued 

 study of ion transport in perfused tissues is planned, and it is hoped that it will lead 

 to a solution of this and other problems raised by the experiments reported here. 



Assuming that tissues in intact animals l)ehave more like perfused tissues than like 

 soaked tissues, we may expect that hypothermia itself will not result in net loss 

 of potassium from the cells. However, other conditions accompanying clinically 

 induced hypothermia may lead to K"^ loss. It has been shown that some of the 

 changes in myocardial excitability in hypothermia may be prevented or diminished 

 by hyperventilation, and are therefore attributable to respiratory acidosis. ^°' ^^ There 

 will certainly 1)e much more said al)out this in some of the papers to follow, and it 

 seems sufficient t(» point out here that acute acidosis is known to produce loss of K* 

 from cells. ^-' ^" 



REFEREXCES 



1. Raker, J. \V., Taylor, I. M., and Hastings, A. B. : Rate of potassium exhange of the 



human erytlirocyte, J. Gen. Physiol. 33: 691-702, 1950. 



2. Sheppard, C. W., and Martin, W. R. : Cation exchange between cells and plasma of mam- 



malian blood. I. Methods and application to potassium exchange in human blood, J. Gen. 

 Physiol. 33: 703-722, 1950. 



