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DISCUSSION 



Talbot : I was most interested, Dr. Davson, in your comments about the 

 cellular oedema that occurs in 'sick' cells. It has been shown that ani- 

 mals deprived of potassium, and thereby subjected to a combination of 

 cellular potassium insufficiency and cellular sodium intoxication, show a 

 tendency to cellular oedema. We therefore wondered whether loss of 

 potassium from the cell was a factor which might interfere with its 

 sodium and water pump mechanisms. 



Davson : We still do not really know what makes a cell stop accumu- 

 lating. Accumulation may be a matter of the development of some 

 anions inside the cell at the same time as the development of a process of 

 excreting the sodium. But if you get rid of sodium, something has got to 

 come in and it may be potassium. That eventually leads to the develop- 

 ment of more of these ions and to a condition in which there is a high 

 potassium concentration inside, and low sodium and chloride. When we 

 allow the system to cool or give it poison, then we find that sodium comes 

 in and potassium goes out ; but when we warm it up again the whole thing 

 reverses and we get back to the original state of affairs. Whether it is 

 that the cell will stop with a given potassium concentration ratio, or a 

 given concentration of sodium, or at a given size, we do not really know 

 for certain. In potassium deficiency, according to the papers I read rather 

 a long time ago, one found that potassium was substituted for by sodium. 



Talbot: That is if sodium is available. 



Davson : So you propose a condition where there is a sodium as well as 

 a potassium deficiency? 



Talbot: You could have simple deprivation with loss of cellular potas- 

 sium, but without entrance of sodium in any appreciable amount. There 

 you have a relatively benign situation. When you superimpose cellular 

 sodium intoxication, things really begin to get mixed up. How do you fit 

 that in with your very interesting observations? 



Davson : It is really a matter of thinking these things out as separate 

 problems as they arise, and there has been no systematic investigation of 

 this. We still have no idea of the mechanism of sodium excretion, and 

 what makes it stop. If one did know more, one would be able to fit in 

 the results with the general physiology of the organism. 



Fejfar: In clinical medicine we now accept that active sodium trans- 

 port and potassium deficiency are very important factors. We assume, 

 when we analyse a muscle biopsy specimen, that we will get a good 



