Abstract
A detailed study of the mechanism of the agglutinating action of salvarsan on red blood cells shows the following points.
In vitro salvarsan has a fairly constant titre of agglutination. There is a progressive drop in this titre as the solution is oxidized on standing. Although the red cells have the power to bind salvarsan in isotonic sugar solutions, no agglutination takes place unless a certain amount of salt is added. Serum, as well as other hydrophilic colloids, under proper conditions may prevent the occurrence of agglutination. It was shown that this inhibition was due to a prevention of the union of salvarsan with the cells.
Salvarsan injected intravenously into rabbits in large doses causes intravascular agglutination which may be observed in the drawn blood. The lungs of such animals are filled with petechial hemorrhages resulting from emboli of the agglutinated red cells, and the animals die acutely.
A certain proportion of animals injected at three-day intervals with sub-lethal doses die during the third or fourth injection in a manner resembling the death of animals injected with large doses. In these animals also the anatomical evidences of intravascular agglutination and pulmonary embolism are constantly present.
The total sum of these repeated doses barely reaches the concentration found necessary for immediate intravascular agglutination, and as this total sum must be considerably reduced by the excretion of salvarsan during the six or nine days intervening, some additional factor must be responsible for the sudden occurrence of intravascular agglutination in these animals.
Examination of their blood shows no increase in the agglutinability of the red cells during the course of the injections, but there is a distinct drop, in some cases to one-sixteenth of the original value, in the power of the serum to inhibit, in vitro, the agglutination of red cells by salvarsan.
Get full access to this article
View all access options for this article.
