Discussion 309 



DISCUSSION 



Fourman: When Dr. Fitzgerald and I started to produce an experi- 

 mental depletion of magnesium we had in mind to do what I had done 

 with potassium (1956. Clin. Sci., 15, 635). But we got nowhere near a 

 significant depletion; only some 70 m-equiv. of magnesium were lost 

 from the body in the course of a month's efforts. Afterwards we realized 

 that this was partly because the urinary and faecal losses became very 

 small when the intake was low. 



Duckworth, Godden and Warnock (1940. Biochem. J., 34, 87) found 

 that the magnesium of bone makes up one-half of the body magnesium. 

 This forms a mobilizable store, which is probably why it is so difficult to 

 produce symptoms of a deficiency of magnesium (Blaxter, K. L., Rook, 

 J.A.F.,andMcDonald, A.M. (1954). J.comp.Path.,64Ao7). A depletion 

 of magnesium seems to bear little relation to what is called a clinical 

 magnesium deficiency by some workers, who have attributed the condi- 

 tion of tremors in patients with alcoholism to a low serum magnesium 

 (Flink et al. (1957). Ann. intern. Med., 47, 956). The plasma magnesium 

 must depend on more than the stores of magnesium in the body. 



Dr. Card, what were the urinary losses of magnesium when you gave 

 the intravenous injections of magnesium? In our experiments, even with 

 the small deficits we had, we found that the urinary losses after injection 

 were less than when the subjects had no deficit. 



Card : I have not got the figures for the amount of magnesium in the 

 urine in the early days of treatment. When you give intravenous mag- 

 nesium some does come through the urine, but these amounts were 

 variable (McCance and Widdowson, 1939). The lowest magnesium we 

 have ever got, without magnesium therapy, was down to 1 m-equiv. /I., 

 and we have taken that as the concentration of the urine prior to mag- 

 nesium therapy. Even that may be too high when a patient is in a 

 deficient state. 



Fourman: It would be very convincing if the injection of magnesium 

 produced little rise in the urinary magnesium, while in normal people it is 

 known to produce a large and prompt rise in the urinary excretion of 

 magnesium. 



Davson: McCance established that the concentration of magnesium 

 in the cerebrospinal fluid was considerably higher than that in the blood 

 plasma. It may be that it is necessary to have a high concentration 

 surrounding the nerve cells to maintain a low level of excitability, in 

 much the same way as there is a low ^concentration of potassium which 

 also decreases with excitability. 



Card: In the experiments where the calves ultimately died, with a big 

 deficit, the tissue magnesium was normal. The whole deficiency appears 

 to occur in the bones, and I think that, as Dr. Fourman suggested, there 

 must be states in which the magnesium is not available. There is one 

 example of magnesium tetany in the literature which is obviously not a 

 case of deficiency, in a child with osteochondritis ; so there may be bone 

 diseases in which this interchange is impossible, and acute states in 

 which magnesium deficiency can occur, entirely different from this 

 chronic deficiency loss. Greenberg and Tufts (1938) went to a good deal 



