Antihaemolytic action of arsenic

Abstract

The foregoing experiments point to certain definite conclusions which may be summed up in a few words.

(1). The entihaercolytic action of arsenic is manifested, and is demonstrable, when the drug is administered in ordinary therapeutic doses. It occurs after the exhibition of arsenic by the mouth, by subcutaneous injection, and by intravenous injection.

(2) . The antihaemolytic effect is rapidly produced, but most rapidly when the arsenic is administered by intravenous injection, being very pronounced within l5 minutes after the injection.

(3). In every case, there is, following the chase of increased resistance, e period in which the resistance of the red blood corpuscles is below normal, the explanation offered being that the arsenic, during the process of excretion, takes with it in combination some part of the cell constituents (lecithin r), thus rendering the cells less perfect and more easily destroyed by the haemolytic agent.

(4). The increase of resistance is as great and as lasting with therapeutic doses as with large toxic doses; the greatest effect being obtained by the intravenous injection of the maximum therapeutic dose.

(5) . After prolonged administration of arseric, the ree' blood corpuscles lose the pro - rerty of increased resistance, and finally no longer react, in that respect, to the subsequent treatment with the drug.

(6) . Sodium Arsenite has a much more powerful effect in producing the antihaemolytic action than Salvarsan (No. 606), and in the minute dose required produces no marked toxic symptoms.

(7) In the condition of paroxysmal haemoglobinuria there is no evidence of a lessened resistance of the red blood, corpuscles.

(8) . Arsenic is not capable, even in solution of 1 in l000, of preventing the lysis of red blood corpuscles by haemolytic blood sera. The significance of this fact is in keeping with the theory that arsenic produces its antihaemolytic action by a chemical combination with the constituents of the red cells..