PAKATHYROID GLANDS 665 



injected had a H-ion concentration greater than pH 6 , tetany did not occur, 

 even though the content of the serum in calcium was decreased. 



The loss of calcium observed during tetany attacks and the discovery 

 that the administration of calcium will ameliorate the symptoms of tetany 

 (MacCallum and Voegtlin, Netter) led many to think that the parathyroid 

 glands exert a direct and specific influence upon calcium metabolism. The 

 tendency at the present time, however, is to look upon the withdrawal of 

 calcium as due to an acidosis, intercalated between it and the hypopara- 

 thyroidism, the body, in its attempts to neutralize the acidosis, catching up 

 ammonia in intermediate metabolism and also, for the same purpose, grad- 

 ually exhausting the stores of the tissue cells in such kations as calcium 

 and magnesium. The marked disturbance in the kation balance in the 

 body thus brought about favors the occurrence of muscular spasms, as we 

 know from the important researches of Sabbatini, Jacques Loeb, J. B. Mac- 

 Callum and S. T. Meltzer (vide supra). 



In the search for the tetany poison, another road has been taken by 

 those who look for it in some derivative of the degradation products of 

 the proteins on the one hand, or of the nucleic acids and mononucleotids 

 on the other. Thus the resemblance of the phenomena of tetany to those of 

 chronic ergotism (Fuchs (a.)) led Biedl to compare the toxic substances in 

 ergot (and the effects they produce) with the hypothetical tetany poison 

 (and the clinical phenomena of tetany). The active principle in ergot seems 

 to be beta-imidazolylethylamin (Barger and Dale), an amino base that is 

 formed when histidin undergoes putrefaction (Ackermann). It seemed 

 possible, therefore, that the tetany poison might consist of amino bases and 

 especially of the base known as beta-imidazolylethylamin. Biedl found 

 that repeated subcutaneous injections of this substance into cats caused an 

 increased excitability of the peripheral nerve trunks, fibrillary twitchings 

 in single muscles, and the peculiar shaking of the paws typical of tetany in 

 cats. Histidin, it will be recalled, is an amino acid of the aromatic series 

 and, in particular, one of the amino acids of the heterocyclic series. 



The question next arose whether derivatives of amino acids of the fatty 

 acid series could be responsible for the origin of a tetany poison. Thus, 

 attention has been directed recently to the guanidino acids that belong to 

 the amino acids of the fatty acid series. The best known member of this 

 group is arginin, which is alpha-amino-delta-guanidino-valerianic acid, 

 whereas histidin is beta-imidazo-alpha-amino-propionic acid. In 1913 and 

 1916 W. B. Koch (a) (b) (c) took up the study of experimental tetany in 

 dogs. In the urine of these dogs he found two guanidin substances, one was 

 methyl cyamidin, the other trimethylamin. These substances, when in- 

 jected into rabbits, produced typical tetany. Koch came to the conclusion 

 that somewhere in the body methyl cyanimid is generated. He believes that 

 this substance has a physiological effect in normal animals, but that, after 

 parathyroid extirpation, it accumulates in toxic quantities and is respon- 



